Thus, stimulation of alternative chloride channels (Xu et al., 2005; Liu et al., 2015; Quesada and Dutzler, 2020) or inhibition of sodium absorption (Blacona et al., 2022) may be able to compensate for the lack of CFTR-mediate Cl− secretion in CF airways or to maximize the efficacy of gene therapies aiming at CFTR. Notably, it was reported that proteasome modulation agent doxorubicin facilitated long-term functional inhibition of ENaC currents. The gene discussed is CFTR; the disease is cystic fibrosis.