Furthermore, in the same experiment, the reduction size of the plaque in the CX3CR1-deficient, CCL2-deficient, and CCL2/CX3CR1-deficient mice was 28%, 36%, and 48%, respectively, with respect to the ordinary Apo E-deficient atherosclerosis model, which suggested that CCL2/CCR2 and CX3CL1/CX3CR1 are independent modulators in atherosclerosis progression. This evidence concerns the gene CX3CR1 and atherosclerosis.