These contradictory findings using the same PPAR-δ knockout construct have been interpreted as suggesting that PPAR-δ has different roles depending on where it is expressed—specifically, that PPAR-δ expressed in noncancerous cells in the tumor microenvironment promotes tumorigenesis, whereas PPAR-δ expressed in cancer cells suppresses tumorigenesis [95]. The gene discussed is PPARD; the disease is cancer.