Among these issues, 1) 19-HETE level needs to be determined during the progression of MASLD; 2) inhibition of COX1/2 seems to ameliorate the function of 20-HETE and thus the physiological role of 20-OH PGG2/PGH2 or 20-OH PGE2 needs to be determined; 3) what role does DCA play in the progression of MASLD, and 4) Can inhibition of the 20-HETE/GPR75 and activation of the 19-HETE/IP2 delay MASLD progression and be a therapeutic option in the treatment of portal hypertension in cirrhosis. This evidence concerns the gene PTGS1 and metabolic dysfunction-associated steatotic liver disease.