And even though the rationale that the effects of atRA on LSCs may explain its clinical effectiveness appears compelling, translation of corresponding laboratory data does not appear straightforward: the impact of EVI1 overexpression on patients’ responses to atRA has not been investigated so far, and the inhibitory effect of atRA alone or in combination with sorafenib on LSCs from FLT3-ITD driven murine AML [16] does not correspond to clinical activity of atRA in FLT3-ITD positive patients [76,77]. Here, FLT3 is linked to acute myeloid leukemia.