We speculate that since prostate (Baena et al., 2013) and potentially stomach adenocarcinoma (Keld et al., 2011) are highly dependent on PEA3 transcriptional dysregulation to enhance tumor progression, the dual loss of CIC and ERF may, in part, represent an alternative mode to de-repress ETS mediated transcriptional programs in these cancer subsets. The gene discussed is ETV4; the disease is cancer.