Tumor cells disrupt the discriminatory functions of the immune response to evade elimination through the following mechanisms: (I) reduced class I MHC expression or genetic loss of B2-microglobulin to prevent cell surface presentation of T cells recognizing tumor-associated antigens (TAAs); (II) tumor cells may inhibit cell-intrinsic activation of pattern recognition receptor (PRR) signaling through the genetic loss or silencing of pathways such as cGAS/STING; and (III) the feedback mechanisms that suppress normal immune responses can be exploited by tumor cells. This evidence concerns the gene CGAS and neoplasm.