These results are in line with Granick et al. (2013), which reported that proliferation of HSPCs in skin wounds in response to Staphylococcus aureus is TLR2-mediated and contributes significantly to the production of neutrophils and resolution of local infection, supporting a role for TLR2 signaling in the regulation of extramedullary hematopoiesis. This evidence concerns the gene TLR2 and infection.