This concern seems to be ruled out by the recent demonstration by De Marchi et al. that pharmacological manipulation of the P2X7R may substantially change immune cell tumor infiltration to the host’s advantage, as administration of a P2X7R blocker to wild-type mice promoted an increase in CD4+ effector cells, but left unaltered the number of CD8+ and Treg cells [19]. The gene discussed is CD8A; the disease is neoplasm.