A study using AML cell lines showed that EVI-1 enhanced the transcriptional response to ATRA [113], and another study using primary samples showed that ATRA induces differentiation and reduces the clonogenic capacity for most of primary EVI-1-positive AML cells in vitro and in vivo, whereas other subtype AML cells lack such a response [114]. This evidence concerns the gene RUNX1 and acute myeloid leukemia.