Studies in mice revealed two interesting features of Muc1 expression: (1) that another transcriptional coregulator, Peroxisome Proliferator-Activated Receptor-γ (PPARγ), stimulates Muc1 expression and (2) Muc1 is expressed by placental trophoblast (Shalom-Barak et al. 2004). PPARγ is activated by various natural ligands including certain polyunsaturated fatty acids and prostaglandin J₂, as well as the synthetic thiazolidinediones, including rosiglitazone and pioglitazone. Investigation of PPARγ actions in human cell lines revealed an opposite response to that observed in mice, namely, inhibition with regard to both progesterone- (Wang et al. 2010) and EGF-simulated (Dharmaraj et al. 2013) MUC1 expression. The human MUC1 gene has a 21 bp insertion in the PPARγ-responsive region which appears to account for the differences in responsiveness between species. In addition to other actions, PPARγ and its agonists have anti-inflammatory actions (Kapadia et al. 2008). In this regard, PPARγ activators can inhibit cytokine-stimulated expression of all three TMs (Fig. 4.2). Therefore, it appears that TM expression can be regulated coordinately offering opportunities for broad therapeutic control. PPARγ activators have therapeutic value in placental dysfunction, including mitigation of symptoms associated with preeclampsia (McCarthy et al. 2011; Kadam et al. 2015). Whether this has relevance to reduction of trophoblast MUC1 expression is unclear.