In Kras-driven genetically engineered mouse models of NSCLC (non-small-cell lung carcinoma) and PDAC (pancreatic ductal adenocarcinoma), dual MEK and ERK inhibition reduced tumor growth and increased progression-free survival, but it is important to note that the animals still died of the tumors, indicating that resistance to dual therapy arises in vivo and that this regime is unlikely to be curative in the clinic [33]. The gene discussed is KRAS; the disease is neoplasm.