Of note, increased succinate production is an inherent property of the CF lung, even in the absence of infection (22), due to a lack of sufficient membrane-bound CF transmembrane conductance regulator (CFTR) and impaired activity of the metabolic regulator Phosphatase and Tensin Homolog deleted on Chromosome 10 (PTEN) (22, 23). The gene discussed is CFTR; the disease is infection.