We read with great attention and intere st the Rapid Review by Kris De Boeck and Margarida Amaral, 1 who suggested a new classification of cystic fibrosis transmembrane regulator (CFTR) mutations on the basis of therapeutic strategies. The proposed classification takes into account the potential of personalised medicine and targeted drugs in the treatment of cystic fibrosis.

The development of new drugs (ie, stabilisers, correctors, or potentiators) based on CFTR gene mutation classes2 is a new and important pharmacological model of precision medicine3 with high financial costs, 4 but the clinical responses so far are variable. Many studies focusing on clinical improvement of cystic fibrosis symptoms through pharmacotherapy include patients with coexisting severe lung disease, which might mask the true effects of the drug being tested. Moreover, patients with the same CFTR mutation genotype can have different drug responses. 2, 5