In accordance with this way of reasoning, the non-canonical binding of Cladosporols into the PPARγ LBD pocket could be the reason for their ability to inhibit adipogenesis in 3T3-L1 cells and also to interfere in the lipid metabolism dysregulation in metastatic PC-3 prostate cancer cells but, at the same time, to limit cell proliferation and migration in HT-29 CRC as well as in PC-3 cells through the inhibition of diverse pathways. Here, PPARG is linked to prostate cancer.