Trisomy of chromosome 11 (+11) is the second most common isolated trisomy in acute myeloid leukemia (AML) patients.1 The presence of +11 is associated with intermediate2, 3 or poor patient outcomes.4, 5, 6 Whereas the clinical characteristics of solitary +11 have been well established,4, 5, 6 relatively little is known about the mutational landscape of sole +11 AML in the age of next-generation sequencing techniques that allow examination of multiple genes relevant to AML pathogenesis.6 So far, the most common molecular feature in AML with isolated +11 is the presence of a partial tandem duplication of the MLL (KMT2A) gene (MLL-PTD), which is detectable in up to 90% of patients.7 Furthermore, a frequent co-occurrence of the FLT3 internal tandem duplication (FLT3-ITD) with MLL-PTD has been reported.8 The aim of our study was to better characterize the mutational landscape of adult AML patients with sole +11.