When the Penninger & Lindeman groups reported their findings, our group was evaluating the alternative but not mutually exclusive hypothesis that RANKL/RANK signaling might operate as a molecular mechanism critical for cell-autonomous maintenance and survival of cellular states with cancer stem cell (CSC)-like properties, including self-renewal, tumor-initiation, drug resistance, and metastasis properties. This evidence concerns the gene TNFRSF11A and neoplasm.