Angioedema is thought to be mediated, at least in part, by BK accumulation and decreased BK metabolism.47 In our study, omapatrilat-treated mice did not exhibit significant BK breakdown, unlike the LisW-S+sacubitril–treated mice, reinforcing the concept that preserving ACE N-domain activity in the presence of NEP inhibition promotes BK metabolism, which may be linked to decreased BK accumulation and vascular permeability and possibly reduced angioedema risk. The gene discussed is MME; the disease is angioedema.