However, disruption in the homeostasis of either bile acid metabolism and/or the microbiome can contribute to HCC development through immune activation and the release of inflammatory cytokines; for example, bacterial translocation in MAFLD patients can activate toll-like receptor 4 (TLR4) via LPS, resulting in inflammatory cytokine production and acceleration of tumor progression [92]. The gene discussed is TLR4; the disease is neoplasm.