Indeed, reactivation of endogenous retroviruses (ERVs) by DNMTi enhances susceptibility to anti-cytotoxic T-lymphocyte-associated protein 4 (CTLA-4) ICI therapy in the B16 mouse melanoma model, a model that has been shown to be highly resistant to ICIs (Fig 1A) [2]. Here, CTLA4 is linked to melanoma.