Although several studies showed that mEHT induces caspase-dependent and independent programmed cell death in various tumor models [20,21,22], in our in vivo model the treatment-induced p53 activation did not lead to apoptosis (neither caspase-dependent nor independent), but it rather induced cell cycle arrest and senescence, marked by the upregulation and nuclear localization of cell cycle inhibitor proteins p21waf1 and p27kip1, which account for the significant tumor growth inhibition. The gene discussed is CDKN1B; the disease is neoplasm.