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The average treatment effect in a target population is $\mathbb{E}[Y(1)-Y(0)]$, the average additive contrast between two potential outcomes. It does not require every individual effect to be the same. If half the population has effect two and half effect minus one, the average treatment effect is $1/2$. Under consistency in causal inference, conditional exchangeability given pretreatment covariates $X$, and positivity, it is identified by ${\mathbb{E}}_X[\mathbb{E}(Y\mid A=1,X)-\mathbb{E}(Y\mid A=0,X)]$. The outer average uses the specified target population, not whichever group happens to be observed most often.

The average treatment effect on the treated is $\mathbb{E}[Y(1)-Y(0)\mid A=1]$, averaging over those who actually receive treatment. Their untreated potential outcomes are counterfactual. This can differ from the average treatment effect when effects vary and treatment uptake changes the population mix. Under conditional exchangeability, consistency in causal inference and adequate untreated overlap, it equals $\mathbb{E}[Y\mid A=1]-\mathbb{E}[\mathbb{E}(Y\mid A=0,X)\mid A=1]$. The second term standardizes untreated outcomes to the treated covariate distribution rather than using the crude untreated mean.

Causal inference uses data and explicit assumptions to learn effects of specified interventions. For binary treatment $A$, a target average treatment effect is $\mathbb{E}[Y(1)-Y(0)]$, comparing potential outcomes for the same population. Observing only $Y=Y(A)$ leaves one of each unit's potential outcomes unobserved.

An observed treated-minus-control difference can include confounding. For a concrete model, suppose half a population is in a low-baseline stratum with $(Y(0),Y(1))=(0,1)$ and half in a high-baseline stratum with $(2,3)$. Let treatment probabilities be $1/4$ and $3/4$ in the two strata. Every unit's causal effect is one. The treated mean is $\frac{1}{4}(1)+\frac{3}{4}(3)=2.5$, while the untreated mean is $\frac{3}{4}(0)+\frac{1}{4}(2)=0.5$. Their observed difference is two because their stratum compositions differ.

Under conditional exchangeability, positivity and consistency in causal inference, outcome standardization identifies the effect byIn the example, using the same half-and-half target weights for both strategies recovers one. The substantive assumptions, rather than the arithmetic alone, justify interpreting the standardized contrast as an intervention effect.^[ref]

The conditional average treatment effect at pretreatment covariates $X=x$ is $\tau (x)=\mathbb{E}[Y(1)-Y(0)\mid X=x]$. It describes average effect variation between strata rather than identifying a particular individual effect. If $\tau (x)=2$ in one equally common stratum and $-1$ in another, the average treatment effect is $1/2$. Under conditional exchangeability, consistency in causal inference and positivity, conditional outcome means identify $\tau (x)$. A predictor measured after treatment cannot simply be substituted for a pretreatment covariate without changing the causal question.

In a binary-treatment potential outcomes model, conditional exchangeability given pretreatment covariates $X$ is $(Y(0),Y(1))\perp A\mid X$. Within each covariate stratum, treatment assignment then carries no information about the relevant potential outcomes. Together with consistency in causal inference and positivity, it permits outcome standardization to identify average causal contrasts. The assumption concerns unobserved counterfactual outcomes and cannot be established just by checking balance of the measured covariates. Including a large list of predictors is not by itself a guarantee that the assumption holds.

G-computation calculates the outcome distribution under a specified intervention from conditional laws identified under a causal model. For a single binary treatment, pretreatment covariates $X$, and outcome $Y$, the G-formula isIt follows by averaging over $X$, using conditional exchangeability to replace the conditional potential outcome mean by the mean among recipients of $a$, and using consistency in causal inference to replace $Y(a)$ by observed $Y$. Positivity ensures the required conditional outcome laws are represented in the target strata.^[ref]

For an illustrative binary outcome, suppose target weights are $0.8$ and $0.2$ in two baseline strata. Untreated risks $0.1,0.4$ give intervention risk $0.8(0.1)+0.2(0.4)=0.16$. Treated risks $0.05,0.2$ give $0.08$, so the standardized causal risk ratio is $0.5$ and the risk difference is $-0.08$. Both strategies use the same target weights.

With repeated treatments and time-varying covariates, the longitudinal G-formula integrates products of the covariate transition laws while setting each treatment according to the intervention strategy. This requires sequential exchangeability, longitudinal positivity and consistency in causal inference. Simply conditioning on every observed intermediate variable can block part of the intended effect; the sequential intervention calculation specifies which laws are averaged.

Inverse probability weighting weights observations by reciprocals of the probabilities that generated their observed assignment or selection. For binary treatment with propensity score $e(X)$, the average-treatment-effect observation weight isIt uses the probability of the treatment actually received. Under conditional exchangeability, consistency in causal inference and positivity, the identification identity isTo prove it, condition on $X$: the assignment probability cancels its denominator, leaving $\mathbb{E}(Y\mid A=a,X)$. Average over $X$ and apply the causal identification assumptions. The same cancellation with a function $g(X)$ instead of $Y$ proves population balance of the measured covariates under correctly specified assignment probabilities.

If a stratum has treatment probability $0.2$, each treated observation there receives weight five: it represents units with the same measured baseline characteristics who usually receive the other treatment. Very small assignment probabilities give large weights and unstable estimates. Estimated assignment models, trimming and normalization can change finite-sample behavior and, for trimming, the target population. Overlap weights deliberately define a different target rather than estimating the same full-population contrast by another name.

Matching constructs comparisons between units receiving different treatments but having similar pretreatment covariates. Similarity can be measured directly on selected covariates or through a propensity score. The design specifies the distance, allowed discrepancies, number of controls per treated unit and whether a control can be reused.

With one distinct control matched to each of $n_T$ treated units, a simple estimator isThis averages differences in the represented treated population. Dropping unmatched treated units changes that population, and reusing controls induces dependence between pair differences. Caliper matching explicitly limits allowed discrepancies.

Matching seeks covariate balance; it does not create a randomized controlled trial. Identifying a causal effect still requires conditional exchangeability given the matched pretreatment covariates, adequate positivity, and consistency in causal inference. Unmeasured determinants of assignment and outcome can remain different even when measured covariates are well balanced. Conditioning on a causal mediator or inducing collider bias is not repaired by calling the procedure matching.

For binary treatment and propensity score $e(X)=P(A=1\mid X)$, the observed-unit overlap weights areEach unit receives the probability of assignment to the opposite group. These weights are bounded between zero and one.^[ref]

The common target-population tilting function is instead $h(X)=e(X)\{1-e(X)\}$. If the original covariate density is $f(X)$, then the unnormalized weighted densities in the two arms are equal:Thus $h$ describes the target population, while $w_1,w_0$ are the arm-specific observation weights. Multiplying every observed unit by $h(X)$ would not give this balance identity.

Under conditional exchangeability, consistency in causal inference and nonzero total overlap, the weighted contrast identifies the overlap-weighted average treatment effectUnits with deterministic treatment assignment have $h=0$ and contribute nothing to this target. The estimand therefore generally differs from the full-population average treatment effect.

Let $Y(1)$ and $Y(0)$ be the potential outcomes for the same individual under well-defined interventions setting the binary exposure to 1 and 0. The average treatment effect, also called the average causal effect on the additive scale, isThe average is over the target population. This compares hypothetical outcomes under two interventions, rather than the observed difference $\mathbb{E}[Y\mid X=1]-\mathbb{E}[Y\mid X=0]$, which can be distorted by confounding. For binary $Y$, the displayed contrast is a causal risk difference. Consistency in causal inference and a well-defined intervention, including an appropriate no-interference in causal inference assumption, give these potential outcomes their meaning.

An instrumental variable $G$ supplies variation in an exposure $B$ that can be used for causal inference about its effect on $Y$. Its three core requirements are:

Relevance, independence, and exclusion are the core instrumental-variable assumptions. They do not by themselves identify an arbitrary population-average effect. For a binary instrument and treatment, instrumental-variable monotonicity and the usual consistency in causal inference assumptions can identify a local average treatment effect; stronger effect-homogeneity or structural-model assumptions are needed for other effect interpretations.

Let $Z$ indicate a recent birthday event, $A$ indicate a social gathering, and $Y$ denote subsequent household COVID-19 infection. The standard instrumental variable conditions are:

The usual consistency in causal inference, well-defined exposure, and absence of relevant interference in causal inference are also needed to interpret the result causally.

The birth-period comparison requires consistency, no interference between individuals, and a real discontinuity in sugar exposure at the end of rationing. Near the cutoff, potential diabetes outcomes must otherwise vary continuously with birth date: no simultaneous policy, nutritional, diagnostic, seasonal, or demographic discontinuity may affect them. Birth dates must not be manipulable around the cutoff, and survival and UK Biobank participation must not create differential selection bias. These assumptions make cutoff assignment locally exchangeable and give a regression discontinuity design an exclusion restriction in which birth period affects diabetes through sugar exposure.

The raw difference is generally not a causal effect. Existing UTCs may differ systematically from non-UTCs in location, admissions, pupil composition, prior attainment, resources, and the local apprenticeship market. These are possible confounders of school type and outcome. The comparison also weights the 43 UTCs and roughly 3500 controls very differently from a clearly defined target population. Without conditional exchangeability, positivity, and consistency, the difference mixes the effect of UTC status with selection bias.

With binary assignment or encouragement $Z$, potential treatment receipt $D(z)$ is the treatment a unit would actually receive under assignment $z$. It differs from the assignment itself when there is noncompliance. Only $D=D(Z)$ is observed for that unit, under the usual consistency in causal inference convention.

The pair $(D(0),D(1))$ defines four principal strata: never-takers $(0,0)$, compliers $(0,1)$, defiers $(1,0)$ and always-takers $(1,1)$. A patient who takes a drug only when encouraged is a complier; one who obtains it under either assignment is an always-taker. Randomization of $Z$ does not itself randomize actual treatment receipt. If $D(1)\ge D(0)$ for every unit, defiers are excluded andunder randomized assignment. Thus the effect of encouragement on uptake identifies the complier fraction, not automatically the effect of receiving treatment on outcomes.^[ref]

A randomized controlled trial assigns experimental units to competing treatments by a specified random mechanism and compares their outcomes. Under complete randomization of $N$ units, exactly $n_1$ receive assignment one and $n_0=N-n_1$ assignment zero. With fixed potential outcomes, each unit has assignment probability $n_1/N$. ThereforeThis proves design-unbiasedness of the mean difference for the finite-population average treatment effect, assuming consistency in causal inference and no interference in causal inference.

Randomization controls the assignment distribution; it does not force every realized baseline covariate difference to be zero. Equal assignment probabilities yield unconditional exchangeability in the design, whereas covariate-dependent randomization can require conditional exchangeability and an analysis respecting that design.^[ref]

When assigned and received treatments differ, an intention-to-treat analysis estimates an assignment-policy effect. A treatment-receipt effect needs additional assumptions. Allocation concealment, blinded outcome assessment and handling of missing follow-up address other sources of distortion beyond random assignment itself.