Schematic representation of critical role of Rac1 in vGPCR paracrine neoplasia. Constitutive stimulation of Rac1 by vGPCR likely leads to phosphorylation of IκB. Phosphorylation targets IκB for ubiquitin-mediated degradation, releasing NF-κB, which then translocates to the nucleus to promote cytokine transcription. Concurrently, Rac1 activation of JNK and p38 may facilitate AP-1–dependent transcription while both Rac1-dependent and -independent signaling pathways may lead to the activation of Akt and the transcription factor NFAT. Transcriptional activation by Rac1 ultimately drives vGPCR paracrine neoplasia.