These activities are likely to be present to at least some degree in many NSCLC tumors and cell lines17,32, as a high proportion of lung cancers express high EZH2 levels and have active CUL-4A, and EZH2 or proteasomal inhibition increased the steady-state level of DLC1 protein in cells where DLC1 is detectable without inhibitor treatment. The gene discussed is DLC1; the disease is lung carcinoma.