The cellular mechanisms attributed to these improvements in bone structure and strength in response to (1) anti‐LRP6 treatment alone, and (2) the anti‐LRP6/DKK1 combination strategy in both naïve and tumor‐bearing conditions, highlights the complex function of potentiated Wnt/β‐catenin signaling on bone remodeling and skeletal metabolism. The gene discussed is LRP6; the disease is neoplasm.