Although it cannot be excluded that increased levels of H3K9me2 upon ZBTB18 expression could result from other co-repressor activities (i.e., specific histone methyltransferases), our data using both LSD1 knockdown and the inhibitor RN1 indicate that, in GBM cells, LSD1 also displays an H3K9me2 demethylase activity, which is important for the LSD1-mediated expression of SCD and SREBF1. The gene discussed is PRDM9; the disease is glioblastoma.