In summary, we propose a possible mechanism for the occurrence of TEs in PNH patients: the abnormal activation and excessive deposition of complement caused by PIG‐A mutation are the basis for the thrombotic tendency in PNH patients, and the mutation/down‐regulation of MUC4 further promotes the deposition of abnormally activated terminal complement C5b‐9 on the cell surface, leading to a severe thrombotic phenotype. The gene discussed is PIGA; the disease is paroxysmal nocturnal hemoglobinuria.