Persons with acquired hemophilia A are often older and suffer from comorbidity or frailty. Little is known about the impact on clinically relevant outcomes of acquired hemophilia A.

We read with interest the article by Taylor et al. [1] describing the laboratory tests, treatment, and course of a hyperfibrinolytic condition during the treatment of rhabdomyosarcoma. The authors stated that bleeding during the treatment of rhabdomyosarcoma was due to hyperfibrinolysis, a condition that should be distinguished from disseminated intravascular coagulation (DIC). However, that case was thought to represent DIC with abnormally enhanced fibrinolysis, so-called enhanced–fibrinolytic-type DIC [2].

The coagulation process relies on an intricate network of three-dimensional structural interactions and subtle biological regulations. In the present review, we illustrate the state of the art of the structural biology of the coagulation cascade by surveying the Protein Data Bank and the EBI AlphaFold databases. Investigations performed in the last decade have provided structural information on essentially all players involved in the process. Indeed, the initial characterization of specific and rather canonical domains has been progressively extended to complicated multidomain proteins.