Similarly, in diabetic ApoE-deficient mice, PKCβ has been demonstrated to contribute to the acceleration of atherosclerosis by modulating the IL-18/IL-18BP axis and MAP kinase signaling pathways, thereby promoting VCAM-1 expression, enhancing macrophage adhesion, impairing endothelial function, and amplifying inflammatory responses in both the aorta and macrophages [58, 59]. The gene discussed is IL18; the disease is atherosclerosis.