In line to these findings, nonetheless, is the observation that Notch action inhibition in H1299 and A549 Kras mutant cells with γ-secretase inhibitor DAPT, alone or in combination with gemcitabine, had a marked effect in NSCLC cell viability and colony-forming potential [123], and that Rumi knockdown, globally inactivating Notch signaling in NSCLC A549 and H23 cells (both Lkb1-deficient [118,124]) results in marked anti-oncogenic exertion, including a significant reduction in cell proliferation, migration and survival [100]. This evidence concerns the gene STK11 and non-small cell lung carcinoma.