This occurred to myoblasts due to increased mTOR activation and reduced autophagy under hyperphosphatemia conditions via Integrin-linked kinase (ILK) activation (Sosa et al., 2018), which is essential to myoblast senescence; suppressing ILK expression resulted in increased autophagy and protected myoblasts from senescence triggered by hyperphosphatemia (Sosa et al., 2018). This evidence concerns the gene ILK and hyperphosphatemia.