By assessing GSE1 levels also in other non-APL AML cell lines, including THP-1, SKNO-1, and OCI-AML2, as well as in an MLL-translocated primary patient sample (BB104) [12] (Fig. S2), we confirmed that the protein downregulation of GSE1 upon LSD1 inhibition was consistent and independent of cellular cytogenetic features. Here, KMT2A is linked to acute myeloid leukemia.