TGFB1 and posterior cortical atrophy: PCa cells in the bone microenvironment disrupt this balance by: 1) over-stimulating osteoblasts to produce new bone, resulting in the production of a weaker woven type of newly formed bone, and 2) by promoting osteoclastogenesis, which leads to excessive osteolysis and the release of large amounts of bone-sequestered growth factors, such as TGF-β, which promote BM-PCa disease progression (3, 4, 7, 8).