Recent studies suggest that G-CSF is an important modulator in inflammatory arthritis [13], [17]–[19], and G-CSF administration has been shown to exacerbate arthritis [20] by increasing the production and mobilization of myeloid lineage cells from the bone marrow [17] and inducing the expression of macrophage antigen-1 (Mac-1) and leukocyte function-associated antigen-1 (LFA-1) on neutrophils to promote leukocyte recruitment at sites of inflammation [17]–[19]. Here, ITGB2 is linked to arthritic joint disease.