However, PARP inhibitor-mediated unrepaired DNA damage may modulate the tumor immune microenvironment and promote responsiveness to ICI through various molecular and cellular mechanisms, such as increased genomic instability, activation of immune pathways, and programmed death-ligand 1 (PD-L1) expression on cancer cells [17], and some studies have supported the use of combination therapy with PARP inhibitor and ICI [18]. This evidence concerns the gene CD274 and neoplasm.