Excitingly, CF therapy has been revolutionizedover the past decadewith the FDA approval of VX-770 (Ivacaftor, Kalydeco) in 2012 forCF patients with the G551D mutation and the following approval ofthree combination therapies for patients with the F508del mutation(Orkambi: VX-770/VX-809; Symdeko: VX-770/VX-661; Trikafta: VX-770/VX-661/VX-445).1 Among these drugs (see Figure 2), VX-770 functions as a potentiator to increasechloride transport through mutant CFTR channels. The gene discussed is CFTR; the disease is cystic fibrosis.