Our observations on the significant associations of GPR55 and CCK with BMI-WHR were also supported by two interesting experimental studies: Compared to wild-type mice, GPR55-null mice exhibited significantly increased fat-mass and insulin resistance as well as decreased spontaneous locomotor activity and physical activity (Meadows et al., 2016); CCK knockout mice were resistant to high-fat diet-induced obesity (Lo et al., 2010). This evidence concerns the gene GPR55 and obesity disorder.