Moreover, Vav1 and PU.1 are recruited to the CD11b promoter in APL-derived promyelocytes, suggesting that the ATRA-induced increase of Vav1 expression and tyrosine phosphorylation may be involved in recruiting PU.1 to its consensus sequence on the CD11b promoter and, ultimately, in regulating CD11b expression during the late stages of neutrophil differentiation of APL-derived promyelocytes [16]. Here, SPI1 is linked to acute promyelocytic leukemia.