ACE2 and inflammation: Sodhi et al. investigated the effects on des-Arg9 bradykinin (DABK) in airway epithelial cells based on a hypothesis that DABK is a biological substrate of ACE2 in the lung, and ACE2 has a significant role in the pathogenesis of acute lung inflammation through modulating DABK/bradykinin receptor B1 (BKB1R) axis signaling.