Interestingly, activation of the ERK and YAP pathways has also been detected in an inflammation-driven model of serrated intestinal tumorigenesis arising through atypical-PKC deficiency, independently of Braf (and Kras) mutations62, signifying that YAP dysregulation may commonly underlie distinct serrated neoplasia pathways independently of the driver mutation. Here, KRAS is linked to neoplasm.