Another hypothesis is consistent with the possibility that the tumors originate from the proliferation of pluripotent fetal Leydig cells (FLCs) that contain ACTH, AII, and Luteinizin hormone (LH)/human Corionic Gonadotrophin (hCG) receptors: the presence of ACTH receptors on FLCs could explain the cell proliferation in males with CAH during fetal life due to chronic exposure to elevated ACTH levels. This evidence concerns the gene PLOD1 and congenital adrenal hyperplasia.