Among the enriched biological process and molecular pathways, we identified that ubiquitin-mediated proteolysis, cardiac muscle contraction, MyD88-dependent Toll-like receptor signaling pathway, and IRE1 alpha-activated chaperones were considered dysregulated and are significant to atherosclerosis progression in FH patients based on kappa statistics and p-values (Figures 7, 8). The gene discussed is MYD88; the disease is familial hyperaldosteronism.