The distinctive structure of atherosclerotic plaque, characterized by calcifications not only in the intima but also in the vascular media, is driven by hyperphosphatemia, disrupted calcium–phosphate balance, elevated FGF23, and reduced level of vascular calcification inhibitors (fetuin-A, matrix Gla protein) alongside a proinflammatory environment exacerbated by HD and chronic associated infections. This evidence concerns the gene FGF23 and Huntington disease.