Studies have shown that hyperphosphatemia can influence the fate of VSMCs by transporting phosphate into VSMCs in a phosphate transporter (Pit1/Pit2)-dependent, independent (in nanoparticle form) or calpain particle (CPP) manner, thereby activating the intracellular pro-calcification signaling pathway and increasing the expression of osteogenic markers Runx2, MSX2, osteogenesis-related transcription factor antibody (osterix), osteopontin and ALP [65, 66]. This evidence concerns the gene RUNX2 and hyperphosphatemia.