 FLT3 genetic alterations include FLT3 somatic point mutations within the second tyrosine kinase domain and internal duplications of the juxta-membrane domain. This alteration is refered to as FLT3-ITD. The FLT3-ITD mutation is found in around 30 of patients with cytogenetically normal AML. Patients with the FLT3-ITD genotype have been reported to have a poor outcome when treated with conventional chemotherapy with an estimated 4-year relapse-free survival of 25 Schlenk et al. N Engl J Med 2008. More recently, the prognostic relevance of FLT3-ITD has been studied in the context of integrated genetic profiling. This confirmed the genetic complexity of AML and also that FLT3-ITD was associated with reduced overall survival in intermediate-risk AML. A multivariate analysis of several genetic alterations revealed that FLT3-ITD was the primary predictor of patient outcome. FLT3-ITD mutations were classified in 3 categories: 1 FLT3-ITD with 8, TET2, DNMT3A or MLL-PTD mutations 3-year OS 14.5; 2 FLT3-ITD with wild type CEBPA, TET2, DNMT3 and MLL-PTD 3-year OS 35.2 and 3 FLT3-ITD with CEBPA mutations 3-year OS 42 Patel JP et al. N Engl J Med 2012. However, FLT3-ITD was not a predictor of response to induction therapy, allowing the introduction of targeted therapies after the induction course. 