In addition to PD-L1 re-expression, the stimulation of IFN production in cancer cells through re-activation of endogenous retroviruses provides an alternative mechanisms for the improved therapeutic efficacy of anti-PD-L1 or anti-CTLA4 and AZA combinations [25,26] in which anti-PD-L1 or anti-CTLA4 therapy contributes to alleviate T cell exhaustion caused by prolonged exposure to AZA-induced IFN. The gene discussed is CTLA4; the disease is cancer.