Nevertheless,based on the observation that bladder cancer appears overrepresented fordual-acting PPARα+γ agonists (Table 1), and direct experimental indication ofcross-talk between PPARα and PPARγ in urothelium as well as other cell types [19, 28, 53–55], ourcurrent hypothesis is that simultaneous activation of PPARα and PPARγ could in some way modulate theproliferation/differentiation balance, contributing to carcinogenesis ofdual-acting PPARα+γ agonists in the rat urothelium (Figure 3). This evidence concerns the gene PPARA and urinary bladder cancer.