This then implies that JMY is playing a dichotomous role in cancer biology: (1) having a tumour suppressive capacity in the event of DNA damage where it enhances p53 activity and (2) functioning as a putative tumour metastasis promoter due to its ability to downregulate E-cadherin, nucleate actin filament and contribute to cell motility. The gene discussed is TP53; the disease is cancer.