1999; Tanaka et al. 2001). In patients with type I CD36 deficiency (homozygote or compound heterozygote of loss‐of‐function mutation), FA uptake is markedly reduced with a robust increase in glucose uptake in the heart‐like CD36−/− mice. Although several reports documented the association of CD36 deficiency to metabolic diseases in humans (Miyaoka et al. 2001; Kuwasako et al. 2003), there is no report showing that CD36 deficiency impairs endurance exercise capacity. The gene discussed is CD36; the disease is metabolic disease.