CaOx exposure can potentiate the upregulation of TGF-β1, which subsequently activates ROS in renal tubular cells; ROS then strongly activates PLSCR, representing one of the major mechanisms by which TGF-β1-ROS signaling stimulates PS externalization in the renal tubule cell membrane during the early stage of kidney stone development. This evidence concerns the gene TGFB1 and nephrolithiasis.