Figure 6 illustrates the binding of lumacaftor, a drug currently approved for cystic fibrosis treatment, to the surface pocket induced by the Val149Gly mutation in human SOD1. PubChem IDs of the tested ligands and their corresponding binding energies are summarized in Table S2. Notably, Val149 plays a critical role in the formation of the functional SOD1 homodimer. Its substitution with glycine is thought to disrupt the dimerization process, thereby contributing to the pathogenesis of amyotrophic lateral sclerosis (ALS) [33]. This evidence concerns the gene SOD1 and cystic fibrosis.