Further applying Seahorse extracellular flux assays, studies have demonstrated that the heightened mitochondrial respiration observed in CF cell lines, including HBE cells expressing CFTRF508del/F508del, can be remarkably normalized by triple CFTR modulator therapy through mechanisms involving calcium (Jarosz-Griffiths et al., 2024). The gene discussed is CFTR; the disease is cystic fibrosis.