This effect may be attributable in part to the ability of these inhibitors to attenuate CD8+ T-cell exhaustion through blocking tumor PD-L1 upregulation [184,185], and in part to the activation of a cGAS/STING-independent, RIG-I-dependent alternative innate immune pathway through concomitant loss of the G1/S and G2/M cell-cycle checkpoints in p53-deficient tumor cells upon ATR inhibition [186]. This evidence concerns the gene CGAS and neoplasm.