At least, our findings suggest that the mechanism underlying the functional differences in the proliferation rates of colorectal cancer cells between the (R) and (S) forms of 13-(Z,E)-HODE [28] may be due to the differential response of enantio-isomers of 13-(Z,E)-HODE to PPARγ-mediated signaling, as the proliferation and apoptosis of cancer cells are regulated by PPARγ [29]. The gene discussed is PPARG; the disease is cancer.