In contrast to the effect of loss of DOK2 in tumors with an EGFR mutation, loss of DOK2 is not consistently associated with KRAS mutation in human lung adenocarcinoma and we do not observe an enhancement of tumor formation in Kras-mutant mice lacking Dok2. Thus the tumor suppressive function of DOK2 in the context of EGFR-RAS signaling lies upstream of RAS, likely through DOK2’s canonical effector, RASA1. This evidence concerns the gene KRAS and lung adenocarcinoma.