Dysbiosis enriched in short-chain fatty acid (SCFA)-producing taxa such as Ruminococcus, Alistipes and Phascolarctobacterium accelerates tumor progression through SCFA-mediated activation of IGF-1/MAPK/PI3K signaling, induction of autophagy and polarization of macrophages toward a tumor-promoting M2 phenotype (32, 33). The gene discussed is IGF1; the disease is neoplasm.