Despite existing evidence for a causal link between Lp(a) and atherosclerosis, the underlying mechanisms are incompletely understood.44,45 Under the oxidation hypothesis of atherogenesis, the initiating element of atherogenesis is the accumulation of oxidized LDL-C in the arterial wall that leads to foam cell formation, triggering atherosclerotic plaque development.46–48 Oxidative stress is a key mechanism in atherogenesis, and ox-LDL has been shown to increase O2.− production by inducing eNOS uncoupling.49,50. Here, NOS3 is linked to atherosclerosis.