Furthermore, cathepsin K is closely related to osteoclast function (being primarily responsible for bone matrix degradation by osteoclasts) and acts as a potential regulator of apoptosis and senescence to control osteoclast numbers in vivo.[12,13] Considering that bone destruction in skeletal metastases may result from osteoclast-induced bone resorption,[14] a CTSK mutation, in this case, will potentially affect the extent of MTC skeletal metastases. The gene discussed is CTSK; the disease is medullary thyroid gland carcinoma.