Furthermore, the loss of tumor suppressors like PTEN or p53, as well as oncogenic mutations in genes like K-ras, c-Myc, and phosphatidylinositol-3 (PI3) kinase, lead to mitochondrial changes that inhibit oxidative phosphorylation (OXPHOS) and promote a metabolic shift toward glycolysis, which supports tumor growth and survival (255). Here, MYC is linked to neoplasm.