Pulmonary thromboembolism in Proteus syndrome, which was observed in our cohort, is elevated relative to the general population and is thought to be due to decreased anticoagulation proteins, venous stasis in vascular malformations, as well as the effects of the pathogenic AKT1 variant on endothelial cells1–3,5,8,10. The gene discussed is AKT1; the disease is Proteus syndrome.