EZH2 and neoplasm: As expected, TAM induction of Ezh2 deletion depleted MYCN, significantly inhibited expression of representative MYCN metabolic targets and uptake of the radiotracer 18F-deoxyglucose (FDG) to tumor sites (Fig. 6e, f), and dramatically prolonged the survival of TH-MYCN mice (Supplementary Fig. 6e).