CDKN1A and neoplasm: In an in vivo model, it showed the potential to arrest the cell cycle, suppress mitosis in tumor, endorse apoptosis, down-regulate pro-survival transcription factors (survivin, Bcl-2, phospho-Akt, c-Myc, mTOR, EGFR, and VEGF), and increase p21/WAF1 activation [230].