A role for CD39 in limiting Th17 cell effector potential has been corroborated by the findings of Morianos et al., who reported that both CD39 and CD73 are required for activin-A-induced suppression of pathogenic Th17 cells in experimental autoimmune encephalomyelitis (Morianos et al., 2020). The gene discussed is ENTPD1; the disease is experimental autoimmune encephalomyelitis.