In this line, it has been shown that loss of SMARCB1 increased recruitment of an endogenous, residual, nuclear SWI/SNF complex and associated histone acetyltransferases (HATs) to target loci, thereby promoting H3K27Ac and thus gene expression that, through Rac activation, enhanced AML cell migration and survival. Here, SMARCA1 is linked to acute myeloid leukemia.