They proposed two potential explanations for the man’s death: reduced myocardial perfusion secondary to Kambô’s hypotensive effects or Kambô-related tachycardia triggering a cardiac arrhythmia in the setting of LVH, both of which could plausibly be attributed to phyllokinin-mediated bradykinin B2 receptor activation, causing systemic vasodilation and hypotension, and sauvagine-induced CRF1 receptor stimulation, contributing to sympathetic overactivity and tachycardia. Here, BDKRB2 is linked to cardiac rhythm disease.