Previous animal studies have shown that various types of chemical colitis models, including DSS, TNBS, and indomethacin models, lead to activation of the kallikrein‐kinin system and bradykinin production in the gut and systemically (Hara et al., 2008; Stadnicki et al., 1998; Wang et al., 2018). This evidence concerns the gene KLK4 and colitis.