We hypothesise that MAGEB2 could act at the level of two mechanisms of action largely mediated by the GAGE family: (i) ability to create a more “open” chromatin structure by up-regulating histone 3 lysine 56 (H3K56Ac) acetylation, which could increase the efficiency of DNA repair, as described in a model of radioresistance in ovarian cancer or (ii) MAGEB2 could promote the development of immunosuppressive EMT (e.g., by down-regulating the expression of CXCL9 and CXCL10) and decreasing the recruitment of effector CD8+ T cells, thereby exerting resistance to checkpoint immunotherapy. The gene discussed is CD8A; the disease is ovarian cancer.