KRAS and cancer: Among the potential synthetic lethal interactors investigated, the suppression of TANK-binding kinase 1 (TBK1) induces apoptosis only in KRAS mutated cancer cell lines via NFκB pathway activation [252], while Syk and Ron kinases and integrin beta6 depletion were able to induce epithelial-mesenchymal transformation (EMT) and apoptosis specifically in KRAS-dependent cells, both in lung and pancreatic cancer [253].