Interestingly, we found that shRNAs targeting the H3K36-specific HMTs, namely SETD2, NSD1, SMYD2, ASH1L, known to conduct the opposite enzymatic activity of KDM2B by catalyzing the addition of methyl groups to H3K36 residues, conferred GBM cells partly resistant to TRAIL-induced apoptosis. The gene discussed is ASH1L; the disease is glioblastoma.