The plausibility of this possibility is increased by the mechanistic relationship between mutant KRAS and low or undetectable DLC1 protein levels in several NSCLC lines that carry mutant or wild-type KRAS. Second, although much of this study has focused on cells that express DLC1 mRNA but lack detectable steady-state DLC1 protein, the phenomenon of EZH2 or proteasome inhibitors increasing DLC1 protein levels was also found to occur in LUAD lines that have detectable DLC1 protein in the absence of inhibitor treatment. The gene discussed is KRAS; the disease is non-small cell lung carcinoma.