In the light of the intimate crosstalk of RAC1/RAC1b and TGF-β signaling in various tumor cell responses and the crucial role of TGF-β in driving the malignant process in both cancer types, it is conceivable that part of the novel RAC1 compound’s efficacy is due to differential inhibition of pro-oncogenic TGF-β responses. The gene discussed is RAC1; the disease is cancer.