Platelet count (PLT) not only play a central role in hemostasis and coagulation but have also been increasingly recognized for their deep involvement in various pathophysiological processes, including inflammation, immune modulation, and tissue repair.[13] The liver is the primary site for thrombopoietin (TPO) synthesis, and impaired liver function can lead to reduced TPO production, thereby affecting PLT counts.[14] In the progression of chronic liver disease, portal hypertension-induced hypersplenism can also accelerate platelet destruction. The gene discussed is TPO; the disease is portal hypertension.