However, it is now clear that in solid tumours, the potency of HDAC inhibitors is critical in determining efficacy; recently the first objective and durable responses in patients with solid tumours (patients with refractory advanced non-small cell lung cancer) were reported using azacytidine in combination with the potent class I HDAC inhibitor, entinostat, and it is now believed that failure of previous trials to demonstrate efficacy was due to the use of less potent HDAC inhibitors [21]. The gene discussed is HDAC9; the disease is non-small cell lung carcinoma.