C1S and hereditary angioedema: The majority of patients with HAE have either a deficiency in C1-esterase inhibitor (type I) or dysfunctional C1-esterase inhibitor (type II), resulting in dysregulation of the kallikrein–kinin pathway and overproduction of bradykinin, which leads to unpredictable episodes of increased vascular permeability, extravasation, and subsequent angioedema attacks [2–4].