Deficiency in LRRC26 or BK pore-forming α-subunit dramatically exacerbates DSS-induced colitis, suggesting a protective role of LRRC26-associated BK channels against chemical-induced colitis in mice, potentially through maintaining normal function of the goblet cells and mucin secretion (Gonzalez-Perez et al., 2021; Fig. 1). Here, LRRC26 is linked to colitis.