Figure 1
![Figure 1. Pie chart depicting the molecular heterogeneity of CN-AML. The analysis is based on mutations in the NPM1, CEBPA, MLL, and FLT3 (ITD and tyrosine kinase domain [TKD] mutations at codons D835 and I836), NRAS, and WT1 genes. Data are derived from mutational analysis of 485 younger adult patients with CN-AML from the German AML Study Group.90](https://ash.silverchair-cdn.com/ash/content_public/journal/blood/119/2/10.1182_blood-2011-08-363291/5/zh89991183350001.jpeg?Expires=1722705885&Signature=w44wuAkBNY5uFa1aPDPDTQdTvFA5WhP8BEytTjze0UosUOpVRbYsBAGiE1WS9JoW4TGMflblkl~ch6bC2DRFfYZK0zeY8nLJmFScUwSkzqEWOZ5HZ-uSRuxJF3gJb6dwPsK1IzADtv3Y9akgFaimj-U~neZLZ~zamAt1t0mxVQK0MG4kW1CtwS17wPmJ9bNF514uEW3vPB2T0-~9ti3E3AN7Ml8yUlOWURTSEThweV9IvpWPnyd4gcdmoaPk988M83kZ23z~AhIIoXt2fhRfPc7mzN0EHExAPyS5E931hsaHVtN554C323UzTlD4hd8VLxH~OlPdAwxkY7w-uRndzA__&Key-Pair-Id=APKAIE5G5CRDK6RD3PGA)
Pie chart depicting the molecular heterogeneity of CN-AML. The analysis is based on mutations in the NPM1, CEBPA, MLL, and FLT3 (ITD and tyrosine kinase domain [TKD] mutations at codons D835 and I836), NRAS, and WT1 genes. Data are derived from mutational analysis of 485 younger adult patients with CN-AML from the German AML Study Group.90
