In vitro experiments, BK channel blocker paxilline, TREK-1 blocker fluoxetine and knockdown of BK and TREK-1 can lead to nasal mucosal dysfunction, which suggests the specific opener to be a potential target for overcoming mucosal remodeling of CRS (Manzanares et al., 2011; Manzanares et al., 2014; Kim et al., 2018). This evidence concerns the gene KCNK2 and congenital rubella syndrome.