To explore whether the increased levels of ∆F508-CFTR due to UBE3C KD could mature into the fully functional form in post-ER compartments, we treated the cells with the CF drug Trikafta, which consists of CFTR correctors VX-661 and VX-445, as well as the CFTR potentiator VX-770 [28]. The gene discussed is UBE3C; the disease is cystic fibrosis.