RARA and acute myeloid leukemia: 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.