The fact that the anti-cancer drug NSC59984, a small molecule known to induce constitutive phosphorylation of ERK2 and reactivate p53 signaling in cancer cells [19, 20], blocked the abnormal proliferation of CCM3-deficient ECs reinforced the hypothesis that some features of CCMs are reminiscent of tumorigenesis [17, 18]. The gene discussed is PDCD10; the disease is cancer.