A team from Spain, China, Switzerland, and the US report on potential treatment targets and resistance mechanisms in KRAS-mutated forms of lung adenocarcinoma. Using genetically engineered mouse model experiments, pharmacological experiments, and other approaches, the team highlighted the potential for curbing lung adenocarcinoma growth by targeting RAF1 as well as cyclin-dependent kinases downstream of the MAP-kinase signaling pathway in advanced tumors driven by KRAS and p53.