The interaction stabilized FOXM1 protein levels and sequentially induced the expression of a series of oncogenes, including MMP-2, VEGF, Chk2, and cyclin D1—a combined body of evidence which may suggest additional roles for PHGDH in glioma tumorigenesis beyond serine biosynthetic flux akin to that described for aKG in a subset of breast cancer cells by Possemato et al. [21] and, in this case, potentially beyond metabolic functions themselves [24]. The gene discussed is FOXM1; the disease is glioma.