Conversely, in MHC‐I‐deficient tumors, NK cells, more than CD8+ T cells were required for effective tumor elimination.[40] Additionally, intratumoral cGAMP treatment of B16‐F10 tumors with high STING protein expression was associated with NK cell‐mediated tumor growth inhibition, whereas in 4T1 breast cancers with low STING expression, cGAMP monotherapy was insufficient to stop tumor growth.[41] These data highlight the indirect effect of STING agonists on NK cell activation in the presence of STING‐expressing tumor cells. The gene discussed is CD8A; the disease is neoplasm.