Importantly, concomitant inhibition of Notch and DDR1 (discoidin domain receptor 1) with GSI LY411575 and 7rh, a benzamide TKI, in Kras-driven murine tumors had an additive effect on apoptosis induction and tumor growth blockage in both p53-proficiency and p53-deficiency contexts, and the co-inhibition of these two pathways with demcizumab (Dll4 blocking antibody) and dasatinib (TKI) markedly reduced tumor growth in Kras-mutant PDX models in a manner comparable to standard cisplatin/paclitaxel chemotherapy [137]. Here, KRAS is linked to neoplasm.