A 19-year-old male with cystic fibrosis (homozygous F508del CFTR mutations, sweat chloride 108 mmol/L) presents with moderate airflow obstruction (baseline FEV1 55% predicted) and recurrent Pseudomonas aeruginosa colonization. He is initiated on elexacaftor/tezacaftor/ivacaftor (Trikafta). The diagram shows his repeat spirometry at 12 weeks. The structure marked **B** in the diagram—a post-Trikafta FEV1 rise of ≥10%—represents a clinically meaningful response. Which of the following best explains the mechanism underlying this improvement in lung function?