Despite the fact that previous studies demonstrated that tumors harboring BRCA1/2 dysfunction and treated with PARPi could increase tumor immunogenicity, therefore sensitizing tumor cells to anti-CTLA4 agents, the whole process remains understudied (Snyder et al., 2014) (Clarke et al., 2009) (McAlpine et al., 2012) (Wen and Leong, 2019) (Brown et al., 2016) (Higuchi et al., 2015). The gene discussed is CTLA4; the disease is neoplasm.