We further demonstrate that p53S upregulated the expression of PGC–1α (also known as PPARGC1A, a PPARG coactivator) and enhanced the interaction between PGC–1α and peroxisome proliferator-activated receptor γ (PPARγ) to increase the number and enhance the function of mitochondria, resulting in increased lipid metabolism, thus inducing cells to escape from cellular senescence and leading to tumor formation. Here, PPARGC1A is linked to neoplasm.