To avoid being recognized by STING-mediated innate immune responses, cancer cells frequently evolve to impede the cGAS–STING signaling pathway, including, but not limited to, downregulating the expression of key signaling proteins (57), limiting STING translocation to the Golgi (6, 46), and mutating the IFN-I locus (48). This evidence concerns the gene STING1 and cancer.