Indeed, a mechanism for ART-driven reservoir stabilization has recently been proposed, namely that uncontrolled HIV infection skews the memory CD4+ T-cell response to a short-lived effector phenotype with lower frequencies of long-lived memory CD4+ T-cells, possibly due to dysregulated IL-7/IL7R signaling (Goonetilleke et al., 2019). Here, IL7R is linked to HIV infectious disease.