STING1 and neoplasm: High-fiber diet-induced microbial alterations derived from STING agonists induced IFN-I signaling via intra-tumour monocytes, shifted mononuclear phagocytes to anti-tumour macrophages (Macs) and triggered monocyte-IFN-I-NK-DC crosstalk, which enhanced anti-tumour responses and ICI efficacy (146).