Tumor onset was markedly accelerated overall in both the p53m/m, nf1b−/−, nf1a+/− (Fig. 2A) and the p53m/m, nf1b−/−, nf1a+/+ backgrounds (Fig. 2B) upon the depletion of suz12. Acceleration of tumor onset in suz12-mutant zebrafish compared to wild-type controls were significant for all suz12-mutant populations, independent of whether one (suz12+/+/+/−), two (suz12+/+/−/−) or three (suz12+/−/−/−) alleles in any combination were disrupted. The gene discussed is NFIB; the disease is neoplasm.