While the aforementioned lack of tumor-like proliferation of CCM2 KO cells may explain the milder course in patients with a CCM2 mutation [88], the high number of CCM3-specific DEGs in ECs indicates a more profound endothelial dysfunction, consistent with a more severe clinical phenotype in patients with a CCM3 mutation [89, 90]. The gene discussed is CCM2; the disease is endothelial dysfunction.