Many studies have suggested that there are two main mechanisms for CPZ-induced coagulopathy: (1) CPZ is hardly metabolized in the body, with about 75% excreted in bile, inhibiting the growth of normal intestinal flora and reducing the synthesis of vitamin K in the intestines; (2) the N-methylthiotetrazole (NMTT) side chain carried by CPZ has a structure similar to glutamic acid, which can interfere with the carboxylation of vitamin K in the liver, thereby reducing the synthesis of prothrombin and lowering the levels of coagulation factors II, VII, IX, and X that depend on vitamin K [18, 19]. The gene discussed is F2; the disease is blood coagulation disease.