In addition to its antineoplastic direct effects against a fraction of the GBM cells, through the promotion of acetylation and cell death, TSA was also able to induce the expression of ligands for the NKG2D- MIC-A and ULBP2- receptors, at both protein and mRNA levels, making these cells susceptible to NK-mediated lysis via TRAIL. The gene discussed is ULBP2; the disease is glioblastoma.