AA is ω-hydroxylated by CYP4A11 and ω-1 hydroxylated by CYP2E1, producing 20-HETE and 19-HETE, respectively, that have opposing physiological roles in the progression of MASLD with CYP4A11-mediated 20-HETE vasoconstrictor activates the GPR75 receptor, which initiates inflammation and divergent un-characterized roles in the progression of MASLD. Here, CYP2E1 is linked to metabolic dysfunction-associated steatotic liver disease.