PRDM2 and cancer: In this multi-cell origin model of cancer initiation [6], inactivation of RIZ1 and upregulation of some oncogenes such as c-Jun in most cells of a diet-responsive tissue may not be sufficient to cause clonal proliferation but may allow a large pool of less than fully normal cells to be more prone to clonal proliferation in response to stochastic strong oncogenic mutations in a single cell.