ΔF508 is the most prevalent mutation detected in patients with cystic fibrosis (CF), and it causes a loss of F508 within CFTR’s first nucleotide binding domain (NBD1). Researchers from Sionna Therapeutics Inc. recently reported the discovery and preclinical evaluation of novel small-molecule CFTR NBD1 stabilizers and CFTR assembly correctors as potential new agents for the treatment of CF.