The decrease in PLT among NAFLD patients aligns with most previous studies[21] and can be attributed to reduced hepatic TPO synthesis, portal hypertension-induced hypersplenism, and platelet consumption in the chronic inflammatory state.[22–24] The elevation in MPV and PDW reflects an accelerated release of larger, newly formed platelets from the bone marrow to meet increased demand, suggesting altered platelet turnover kinetics in the pathological process of NAFLD, potentially linked to inflammation and tissue repair processes.[25,26]. This evidence concerns the gene TPO and metabolic dysfunction-associated steatotic liver disease.