Its mode of action in DCs is mediated via multiple mechanisms, including limiting the activation of the cGAS-STING pathway [84], which is necessary for cross-presentation of tumor-associated antigens [85, 86], mediating T-cell trogocytosis which labels these cells as a target for fratricide T-cell killing [87], or preventing increased exposure of intratumoral CD8+ T cells to DC-derived chemokines and cytokines, namely CXCL9 and IL-12 [88]. This evidence concerns the gene CGAS and neoplasm.