In cancer cells, IFN-I may act within a state of “viral mimicry” which is characterized by the accumulation of cytosolic DNA induction, activation of the cyclic GMP-AMP synthase (cGAS)/stimulator of IFN genes (STING) pathway, reactivation of immunogenic cancer antigens, increased HLA-class I-restricted antigen presentation, and downstream production of IFN-I and pro-inflammatory cytokines [27,28]. This evidence concerns the gene CGAS and cancer.