Consistent with the coactivator having tumor-suppressive functions, Lee et al. showed that overexpression of PGC-1α increases the epithelial marker E-cadherin and reduces motility of HepG2 cells possibly through PPARγ [194] and PGC-1α can bind p53 and enhance transcription of proarrest genes including cyclin-dependent kinase inhibitor 1 (p21), growth arrest and DNA damage-inducible 45 (GADD45), TP53-inducible glycolysis and apoptosis regulator (TIGAR), SCO cytochrome C oxidase assembly Protein 2 (SCO2), and sestrin2 in human hepatoma cells [195]. The gene discussed is TP53; the disease is neoplasm.