In the context of mitochondrial function and its susceptibility to oxidative stress, aconitase, a key enzyme in the Krebs cycle, has demonstrated altered activity in CF models, including a notable loss of mitochondrial aconitase activity in FABP Cftr-KO mice and a decrease in CFTR-deficient lung cells, highlighting its vulnerability to oxidative damage in CF (Velsor et al., 2006). The gene discussed is CFTR; the disease is cystic fibrosis.