However, in atherosclerosis, the role of Th2 inflammation was still confused yet: when targeted deletion of Th2 cytokine, IL-5, atherosclerosis progression was accelerated, which proposed an athero-protective role of Th2 inflammation (48); when targeted deletion of Th2 cytokine, IL-4, the ApoE−/− mice and LDLR−/− mice developed less severe atherosclerotic, which implied a proatherogenic function of Th2 inflammation (49, 50). This evidence concerns the gene IL4 and atherosclerosis.