In an experimental study [70], CIH + a high-cholesterol diet (HCD) induced AS development, whereas knockdown of the NF-κB P50 subunit eliminated the AS lesions induced by CIH + HCD by significantly inhibiting three major atherogenic mechanisms: vascular inflammation, hypercholesterolemia, and macrophage foam cell formation. Here, NFKB1 is linked to Hypercholesterolemia.