Critically, genetic interaction studies have recently demonstrated that Notch1 activation is indeed required for Kras-triggered lung adenocarcinoma formation and NSCLC regulation of cell survival through modulation of p53 [88], and it has been shown that pharmacological inhibition of Notch signaling with GSI LY411575 suppresses Kras-driven lung adenocarcinoma tumor growth [87]. This evidence concerns the gene KRAS and lung adenocarcinoma.