However, contradictory outcomes for the anti‐tumor efficacy of genetic or therapeutic targeting of the Notch1 pathway in oncogenic KRAS‐driven LAC, along with our own current data showing no alterations to Notch1 activity upon ADAM17 targeting in mutant KRAS LAC models, raise questions over the role of Notch1 as a driver of this oncogenic setting (Ambrogio et al, 2016). This evidence concerns the gene ADAM17 and neoplasm.