Inosine activation of the A2AR on T cells is itself complex: inosine either prevented Th1 differentiation and blunted anti-tumor immunity in anti-CTLA4-treated mice or, conversely, enhanced both, when co-supplied with IFNγ in vitro and a TLR9 agonist in vivo (Mager et al., 2020). The gene discussed is IFNG; the disease is neoplasm.