Data from combined cytokine studies, neutralization experiments, and proliferation assays unveiled that induction of CD8(+) Tregs under in vitro conditions relies at least partially on TGF-β1 to exert their suppressive function, a process that is critically mediated by activation of p38MAPK, suggesting p38MAPK as a potential therapeutic target in ovarian cancer immunotherapy (Wu et al., 2016a). Here, CD8A is linked to ovarian carcinoma.