It is known that most of the kinase inhibitors are heavily metabolized both at the hepatic and the tumor level, but the role of metabolism in prostate tumor response to KIs has not been investigated in details, in particular the role of the pregnane X receptor (PXR) that regulates the expression of a large set of DMET genes involved in the metabolism of a large panel of xenobiotics [18]. This evidence concerns the gene NR1I2 and prostate neoplasm.