Recently, however, it has been reported that Csf-2r-deficient (Csf2rb−/−Csf2rb2−/−) mice that lack the common β subunit (Csf2rb) and the IL-3r unique β subunit (Csf2rb2) were equally efficient as WT mice in controlling L. monocytogenes bacterial burden in the spleen and liver early after infection [44]. This evidence concerns the gene CSF2RBP1 and infection.