Growth and proliferation potentiated by deregulated myc oncogene expression is balanced by myc-induced apoptosis. Abrogation of this apoptotic pathway in Myc overexpressing cells leads to cancer progression. Recent work has shown that cell clones in the Drosophila wing disc with higher dMyc expression levels act as supercompetitors to potentiate the programmed death of surrounding normal cells. Yet another paper identifies dE2F1 as a critical component of pathways that normally restrict the ability of growth perturbing genes like dMyc to cause organ overgrowth.