found that PTEN negatively regulated the G1/S phase transitionby obstructing S-phase kinase-associated protein-2 expression (SKP2)and ultimately alleviating the levels of p27/CDKN1B.500 In GBM, loss of PTEN causes the activation of FAK and apoptoticresistance due to the absence of contact (cell–matrix). The gene discussed is CDKN1B; the disease is glioblastoma.