Interestingly, serum amyloid A, which is a major acute-phase protein that is secreted from liver cells in response to infection or injury, blocks M-CSF/c-Fms signaling via activation of p38 and ERK, thus inhibiting osteoclast formation by repressing osteoclast-associated genes, such as RANK and TRAF6, and inducing expression of anti-osteoclastogenic genes, such as MafB and the gene encoding interferon regulatory factor 8 [105]. The gene discussed is MAPK1; the disease is infection.