We found that Foxp1 can associate with the Foxp3 locus upon TGF-β treatment, first with its promoter, followed by the enhancer region CNS2. The stepwise pattern of binding, along with previous findings where Foxp1 was reported as an integral part of Smad signaling pathway in tumor-infiltrated CD8+ T cells, strongly indicated that its initial recruitment to Foxp3 promoter is likely a Smad-dependent event. Here, FOXP3 is linked to neoplasm.