The results presented here implicate that Ifrd1 and Ifrd2 play a up to now unknown role in the regulation of Cd36 and therefore possibly contribute to Cd36-related pathogenesis of human metabolic diseases, such as hypoglycemia (Nagasaka et al., 2011), hypertriglyceridemia (Kashiwagi et al., 2001), and disordered fatty acid metabolism (Glazier et al., 2002; Tanaka et al., 2001). This evidence concerns the gene IFRD1 and metabolic disease.