“…In type IIa, mutations affect the reactive site, in type IIb, mutations affect the heparin-binding site and in type IIc, mutations show different defects in other parts of the protein [ 3 ]. Independent of its classification, AT deficiency, with a prevalence of 0.1–0.3% within the Caucasian population, poses a major risk for thromboembolic events [ 4 , 5 ].…”