This phenomenon may be attributed to L-FABP’s capacity to influence FAs metabolism through peroxisomeproliferator-activated receptor α (PPARα) (Pawlak et al., 2015) and expedite the progression of NAFLD by promoting steatosis and activating hepatic stellate cells (HSC) (Newberry et al., 2012; Chen et al., 2013). Here, FABP1 is linked to metabolic dysfunction-associated steatotic liver disease.