Our findings support a tumorigenesis model where NMNAT proteins promote glioma growth through regulating NAD+-dependent PTM of p53, and driving cellular pools of p53 toward PARylated-p53 (inactive p53) and away from acetyl-p53 (active p53) to ameliorate DNA damage-triggered cell death under oncogenic stresses associated with tumor development (Figure 11E). The gene discussed is TP53; the disease is central nervous system cancer.