Hereditary angioedema (HAE) is a rare genetic disorder characterized by recurring episodes of subcutaneous and/or submucosal edema without urticaria due to an excess of bradykinin (1, 2). HAE is classified into 2 main types (1). Type I HAE is caused by deficiency of C1 esterase inhibitor, accounting for 85% of cases (1). Type II HAE occurs in only 15% of cases and is marked by normal to elevated levels of C1 esterase inhibitor but with a reduction in activity (1). An angioedema attack can range in severity depending on the location and degree of edema (2). Furthermore, patients with HAE are often diagnosed with anxiety and depression secondary to their poor quality of life (3). Thus, long-term prophylaxis of attacks can be crucial to reduce the physical and psychological implications. For long-term prophylaxis, lanadelumab, a subcutaneously delivered monoclonal antibody inhibitor of plasma kallikrein, has been proven to decrease the frequency of HAE attacks without significant side effects (4). However, data is limited, specifically regarding patients with type II HAE and patients >/= 65 years (4).