Since macrophage plays a crucial role in the pathogenesis of atherosclerosis and LB100 treated experiments suggested that inhibition of PP2A activity mainly affected lipids deposition, we decided to produce mice with conditional knockout of the PP2A-Cα subunit in myeloid cells by crossbreeding CreLyz2 and Ppp2cαflox/flox (fl/fl) mice to investigate whether PP2A deficiency in myeloid cells accelerates the progression of atherosclerosis. This evidence concerns the gene PTPA and atherosclerosis.