Both PPARγ and PPARδ nuclear receptors are assumed to promote the growth of both normal colonic crypt cells and CRC.(37,38) PPARγ down-regulation induced by antagonist- or RNA interference causes apoptosis via reduction of cellular adhesion molecule expression.(39) We recently found that FuOH induced anchorage-dependent apoptosis, anoikis, through modification of integrin signals in adherent human CRC cells (data not shown). The gene discussed is PPARG; the disease is colorectal carcinoma.