One mechanism by which dysregulated Rac1 signalling may promote tumourigenesis is by modulating the activities of various transcription factors, including nuclear factor-kappa B (NF-κB), activator protein-1 (AP-1), and signal transducer and activator of transcription 3 (STAT3), which regulate the transcription of genes involved in tumourigenic events such as cell proliferation, tumour angiogenesis, and cell survival [reviewed in [9]]. This evidence concerns the gene STAT3 and neoplasm.