Besides a shortening of the BCL2 half-life, which has been implicated as a resistance mechanism in AML [3, 5, 8, 10], an additional potential pathophysiological mechanism of the anti-leukemic activity of ATRA was described by Balusu et al. in AML with mutant NPM1 [11]. This evidence concerns the gene BCL2 and acute myeloid leukemia.