In line with these findings, in a model of medulloblastoma, Bolin et al. showed that CDK2 inhibitor milciclib strongly synergized with BETi in downregulating c-MYC, leading to cell cycle arrest and apoptosis and to prolonged survival of mice orthotopically injected into the cerebellum with medulloblastoma cells [200]. The gene discussed is CDK2; the disease is medulloblastoma.