Excessive osteoclast activity could cause imbalanced bone homeostasis, resulting in metabolic skeletal diseases, such as metastatic cancers, rheumatic arthritis, and osteoporosis.55,56 Research has shown that osteocyte death caused by the stimulation of macrophage-inducible C-type lectins can stimulate osteoclast formation and aggravate bone loss.57 Additionally, Vav3,58 semaphorin 3 A (SEMA3A),59,60 and protein kinase C beta II (PKCβII)61 were demonstrated to regulate osteoclast formation and bone loss. The gene discussed is CLEC4E; the disease is bone disorder.