In a bone fracture mouse model, Egr1 deficiency leads to several bone defects including persistant fibrin accumulation in the fracture gap, abnormal callus ossification with enlarged areas of cartilaginous tissue, decreased expression levels of Bglap (Osteocalcin), and bone resorbtion markers that regulate extracellular matrix, including Acp5 (Tartrate-resistant acid phosphatase) and Ctsk (Cathepsin K) genes [93,118]. Here, CTSK is linked to bone fracture.