Our previous studies have proved that high level DCA could act as damage-associated molecular pattern (DAMP) to trigger NLRP3 inflammasome activation in macrophages, meanwhile, excessive DCA could also trans-activate toll-like receptor 2 (TLR2) and downstream signaling, promoting M1 macrophage polarization as well as pro-inflammatory cytokines production and therefore participating in the HFD-related colonic inflammation [15, 16]. The gene discussed is TLR2; the disease is colitis.