Inhibition in task switching is inferred from slower reaction times returning to a recently performed task after one intervening trial (i. e. an ABA sequence) compared to returning to a task not recently performed (CBA sequence). These n-2 repetition costs are thought to reflect the persisting inhibition of a task after its disengagement. As such, the n-2 repetition cost is an attractive tool for the researcher interested in inhibitory functioning in clinicaleurologicaleuroscience disciplines. In the literature, an absence of this cost is often interpreted as an absence of inhibition, an assumption with strong implications for researchers. The current paper argues that this is not necessarily an accurate interpretation, as an absence of inhibition should lead to an n-2 repetition benefit as a task's activation level will prime performance. This argument is supported by three instances of a computational cognitive model varying the degree of inhibition present. An inhibition model fits human n-2 repetition costs well. Removal of the inhibition-the activation-only model-predicts an n-2 repetition benefit. For the model to produce a null n-2 repetition cost, small amounts of inhibition were required-the reduced-inhibition model. The authors also demonstrate that a lateral-inhibition locus of the n-2 repetition cost cannot account for observed human data. The authors conclude that a null n-2 repetition cost provides no evidence on its own for an absence of inhibition, and propose reporting of a significant n-2 repetition benefit to be the best evidence for a lack of inhibition. Implications for theories on task switching are discussed.
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