Since previous studies using liver-specific CaMKII-deleted mice showed that CaMKII mediated the suppression of insulin signaling and increases in glucose neogenesis in the livers of obese mice [13, 14], we cannot rule out the possibility that KN-93 and acremomannolipin A attenuated glucose intolerance by inhibiting CaMKII in the livers of obese mice. This evidence concerns the gene CAMK2G and Glucose intolerance.