CaMKII plays a critical role in the molecular mechanism that regulate atherosclerotic plaque progression. The crosstalk between macrophages and VSMCs is regulated by CaMKII in atherosclerotic lesions. CaMKII levels are increased in stable plaque (SP), while unstable plaque (UnSP) have increased expression of CaMKIV. This study contributes to the understanding of the molecular mechanism underpinning atherosclerotic plaque progression.