Additional interaction nodes between YAP1 and KRAS pathways that have been suggested include (i) the convergence of both pathways on the activation of the induction of epithelial–mesenchymal transition (EMT) via the transcription factor fos proto-oncogene (FOS), (ii) the KRAS-mediated stabilization of YAP1 via the downregulation of SOCS-box proteins and (iii) the role of YAP1 as an oncogenic KRAS effector in TRP53 mutant pancreas tumor [15,18,19]. This evidence concerns the gene KRAS and pancreatic neoplasm.