Interaction analysis showed that ACTB formed the hub of the revealed network, being involved in many interactions with other accessory proteins (e.g., with upregulated CAP1, WDR1, GSN, RHOA, and ARPC1A), suggesting myocardial cytoskeleton rearrangement in response to hypercholesterolemia. This evidence concerns the gene ARPC1A and familial hypercholesterolemia.