“…The ‘anabolic’ and ‘catabolic’ effects of relaxin on bone metabolism probably depend on dose and timing of administration, and modulating RXFP1 receptor expression by bone cells would represent a key strategy favouring either bone formation, in the case of osteopenia or osteoporosis, or bone resorption, in the case of ectopic calcification or undesired abnormal bone deposition (Duarte et al , ). It should be noted that eventual treatment with relaxin should be considered with caution, because it has relatively recently emerged that relaxin signalling is involved in human cancers, in particular in mammary (Tashima et al , ), prostate (Feng et al , ; Vinall et al , ) and thyroid cancer (Hombach‐Klonisch et al , ; Bialek et al , ) and osteosarcomas (MA et al , ; Huang et al , ; Marioni et al , ). In this regard, relaxin is thought to be involved in metastatic tumour‐driven osteolysis, in which there is increased osteoclast activity.…”