These result in several classes of protein dysfunction, affecting CFTR (I) synthesis, (II) maturation, (III) regulation, (IV) conductance, (V) quantity, and (VI) stability (Figure 1; Tildy and Rogers, 2015), The most common mutation is F508del (class II), which exists in ∼70% of CF patients (Rowntree and Harris, 2003). The gene discussed is CFTR; the disease is cystic fibrosis.