CGAS and neoplasm: The tumor microenvironment (TME) is a central mediator of immune resistance, involving: cancer-associated fibroblasts (CAFs) (7) and tumor-associated macrophages (TAMs) secreting immunosuppressive factors to recruit inhibitory immune cells (8); lactate accumulation due to metabolic reprogramming suppressing CD8+ T cell function (9); and cGAS-STING pathway dysregulation – where chromosomal instability (CIN) in TNBC can activate cGAS-STING signaling, but the induced IL-6/STAT3 axis counterintuitively promotes tumor survival (10).