Recent studies have identified that the loss of TET2 in mice predisposed to atherosclerosis due to knockout of the low-density lipoprotein receptor (Ldlr) express higher levels of proinflammatory genes, such as Il1b, Il6, Cxcl1, Cxcl2, and Cxcl316,26. The gene discussed is LDLR; the disease is atherosclerosis.