Activation of ACSL1 is associated with enhanced tumor cell proliferation, migration, and resistance to oxidative stress.[51] In ulcerative colitis models, ACSL1 can work with CPT1A to promote FAO and M2 macrophage polarization through the PPAR-γ signaling pathway.[52] In conclusion, based on its structural characteristics and metabolic properties as a MUFA, we hypothesize that 5-dodecenoic acid may influence energy metabolism and cell fate in EC by acting through fatty acid metabolism pathways involving CPT1A and ACSL1. The gene discussed is PPARG; the disease is neoplasm.