Since ERK activity is often correlated with the cells ability to proliferate, such as the case in cancer [33,34], the endothelial or vascular progenitor cell that contains the causative DUSP5 somatic mutation is likely to lose the ability to negatively regulate pERK, thus causing endothelial cell to hyperproliferate, and display the vascular anomaly phenotype. The gene discussed is DUSP5; the disease is cancer.