Indeed, the RNAseq analysis of a large set of AML patients confirmed that AML cells overexpressed SMARCA5 and its levels correlated with many ISWI-complex members including also cohesin complex, and finally, that the proliferative nature of AML cells marked by upregulation of SMARCA5 was supported by a trend in shorter OS albeit only in those AML patients that were marked by cytogenetic aberrations (see Figure 1). The gene discussed is SMARCA5; the disease is acute myeloid leukemia.