Relevant studies have shown that even small mutations in SERPINC1 can cause hereditary AT III deficiency, and almost all deletions and nonsense mutations lead to hereditary AT III deficiency of type I.[16–19] The SERPINC1 mutation c.331 T > C in this patient was firstly reported in 2017, which was classified into type I AT III deficiency with AT III activity of 49% and mean AT antigen of 52%.[5] We further conducted gene mutation and protein function prediction whose results revealed the mutation was harmful. The gene discussed is SERPINC1; the disease is hereditary antithrombin deficiency.