However, our findings, combined with the fact that RNF5 is a current drug target in CF patients because its downregulation contributes to stabilizing and rescuing the function of mutant CFTR proteins (Sondo et al., 2018; Tomati et al., 2015), suggests that the association between 8.1AH CF carriers and delayed bacterial colonization could be due to decreased expression of RNF5 (Lyczak et al., 2002; Mall and Hartl, 2014; McNicholas, 2017; Pier et al., 1996). This evidence concerns the gene CFTR and cystic fibrosis.