In vitro experiments with AML cells suggested a role of BM stroma in degrading atRA: human AML cell lines with different driver lesions (PML-RARA, AML1-ETO, NPM1 mutations), as well as primary samples expressing AML1-ETO or related fusion genes, responded to atRA by differentiation and/or loss of clonogenic activity. This evidence concerns the gene RUNX1T1 and acute myeloid leukemia.