CGAS and colorectal carcinoma: These pressures are compounded by TP53-associated chromosomal instability, which generates micronuclei capable of activating cGAS–STING and innate sensing; in CRC, however, such signals are frequently buffered by a TGF-β–rich, myeloid-skewed, immune-excluded microenvironment that limits effector trafficking [23,24,33,34,35].