For a typical instance, it has been demonstrated that valproic acid, which has been used for the treatment of depression and epilepsy such as tonic-clonic seizures, contributes to the up-regulation of CDKN1A/B (p21/CIP1/WAF1, p27/KIP1) and down-regulation of c-Myc, thereby augmenting mammalian target of rapamycin (mTOR) inhibitor to induce autophagic cell death in cutaneous T cell and Burkitt lymphomas [74–76]. This evidence concerns the gene MTOR and Burkitt lymphoma.