Susceptibility to experimental atherosclerosis in APOA1 or LCAT ablated mouse models requires an additional mutation, such as apoE deficiency or LDL receptor deficiency (33, 34) and even then may involve decreased PON1, whereas PON1 knock-out mice are prone to atherosclerosis induced simply with atherogenic chow even without cross-breeding with apolipoprotein E (apoE) ablated mice (35). Here, PON1 is linked to atherosclerosis.