Altogether, tumor cell PD-L1 expression is controlled by the STAT-IRF pathway which is regulated by distinct DNA damage mechanisms: 1) DSB-induced ATM/ATR/CHK1 kinase activities, 2) DDR deficiency/high MSI/increased TMB resulting in neoantigen-induced T cell activation and IFN-γ production, and 3) cytosolic DNA fragments that induce the cGAS/STING pathway resulting in type I interferon activity (68). This evidence concerns the gene SOAT1 and neoplasm.