With the goal of developing a gene therapy reagent for cystic fibrosis (CF), many strategies to improve AAV vector transduction and gene expression in airway epithelial cells have been advanced, such as improved capsid design (Excoffon et al., 2009; Limberis et al., 2009), a short but strong promoter (Yan et al., 2015), shortened CFTR cDNA (Ostedgaard et al., 2005), and incorporating proteasome modulators to increase AAV genome trafficking to the nucleus (Zhang et al., 2004). The gene discussed is CFTR; the disease is cystic fibrosis.