In our previous studies, we identified that the bone-metastatic RCC cells were able to secrete significantly more stress-induced phosphoprotein 1 (STIP1) protein than the primary RCC cells 29, not only promoted the proliferation and migration/invasion of RCC tumor cells through the autocrine receptor, but also facilitated the differentiation of osteoclasts and up-regulated cathepsin K through paracrine, to degrade collagen and other matrix proteins during bone resorption 29. This evidence concerns the gene STIP1 and neoplasm.