This evidence was supported by the experimental study on atherosclerosis-susceptible B6 (B6.apoE -/-) and atherosclerosis-resistant BALB (BALB.apoE -/-) mice that showed defects in insulin secretion rather than defects in insulin resistance which explains the mark difference in susceptibility to T2DM [45]. The gene discussed is APOE; the disease is type 2 diabetes mellitus.