Mechanistic studies in lung cancer have revealed that DNM3 interacts with growth factor receptor–bound protein 2 (GBR2), thereby interrupting the formation of a complex between tyrosine-protein kinase Met (c-MET), GBR2, and signal transducer and activator of transcription 3 (STAT3), which in turn suppresses STAT3 activation [46]. This evidence concerns the gene STAT3 and lung cancer.