Nf1/Kras double-mutant mice have been shown to develop myeloid malignancies with reduced latency and increased severity in comparison to mice with only one of the two defects because copy number variations (CNVs) in Nf1/Kras mutant mice frequently resulted in haploinsufficiency for PRC2 core subunits (SUZ12 or EZH2) or PRC2-associated factors necessary for optimal PRC2 activity (AEBP2, CDYL or JARID2) [92]. The gene discussed is KRAS; the disease is myeloid neoplasm.