For example, CD62L expression by peripheral CD8+TM generated in response to an acute pathogen challenge is progressively enhanced as a function of original priming conditions and infection history; upon entry into certain lymphoid or nonlymphoid tissues, CD8+TM-expressed CD62L is reduced; and CD8+TEM and TCM subsets themselves are subject to gradual adaptations that introduce an array of molecular, phenotypic and functional changes including, importantly, an increase of their respective recall capacities [2, 5–10]. Here, CD8A is linked to infection.