Another previously unrecognized gene that appears to play a role in CCM formation is Pten (phosphatase and tensin homolog on chromosome 10).[64] Pten is known to play a crucial role in the regulation of cell growth and proliferation as well as programmed cell death.[17, 29, 33] Work by Zhu et al. demonstrates that Pten loss may occur in up to one-third of the endothelial cells within the CCMs, particularly in cases where the lesions are multiple and/or small. The gene discussed is PTEN; the disease is cerebral cavernous malformation.