These observations raise the intriguing possibility that the tumor suppressive activities of KLF2 may originate from the ability of this factor to control the transcriptional activity of RA and that it does so by shifting RA signaling from the pro-oncogenic FABP5/PPARβ/δ to the anti-carcinogenic CRABP2/RAR path. The gene discussed is KLF2; the disease is neoplasm.