Previous studies have demonstrated that PKA RIIβ deficiency enhances energy expenditure and protects mice from obesity, insulin resistance, and dyslipidemia.[12, 28] However, PKA may not be an ideal drug target for obesity since whole‐body knockout of RIIβ has markedly diminished WAT despite normal food intake, which often causes serious health problem under certain circumstances.[11] Interestingly, our data showed that the knockout of AKAP1, the scaffold protein that anchor PKA onto mitochondria, resulted in a different lean phenotype when compared to RIIβ knockout mice. This evidence concerns the gene AKAP1 and obesity disorder.