In this regard, Fons et al. (2019) demonstrated that mutant PPM1D, a protein phosphatase often found truncated in pediatric gliomas, drives hypermethylation of CpG islands throughout the genome and promotes epigenetic silencing of NAPRT, conferring NAMPT inhibitor sensitivity in glioma and revealing a promising approach for the targeting of PPM1D mutant tumors. The gene discussed is PPM1D; the disease is central nervous system cancer.