A lack of Fos abolishes osteoclastogenesis and induces osteopetrosis in mice,84 while the overexpression of Fos reverses the OPG-mediated suppression of osteoclastogenesis.85 In summary, prolonged exposure to inflammatory signals in TLR9−/− mice may sustain higher expression and transcriptional activity of Fos and Spi1 in progenitors during myelopoiesis and monocyte differentiation. Here, TLR9 is linked to osteopetrosis.