These different results can be partially explained by differences in the studies such as the species, type of PPAR agonist, method to induce hepatic steatosis, the type of genetic strategy used to induce PPARγ overexpression or deficiency in PPARγ expression as well as differences in the pretreatment times of the drugs used (see Table 1). The gene discussed is PPARG; the disease is Hepatic steatosis.