However, our unpublished data show that either endogenous or exogenous RANKL directly stimulates the proliferation and enhances the invasiveness of human trophoblasts, partially echoing its role in tumor cells.19 We propose that the lack of RANKL in vivo may result in a decrease in trophoblast proliferation and invasion, but to a certain extent, it will also create a proinflammatory microenvironment. Here, TNFSF11 is linked to neoplasm.