Thus, the basal level of M-CSF is required to maintain the homeostasis of tissue macrophage through M-CSF signaling, while the local and temporal increase in GM-CSF, which inhibits M-CSF signaling during inflammation, polarizes monocytes to differentiate into inflammatory Mφ during the inflammatory reaction and shift back to resting macrophages after the infection-induced inflammation is removed [4]. This evidence concerns the gene CSF2 and infection.