Consistent with this hypothesis, previous studies using mice expressing a C-terminally truncated SOCS3 that lacks the SOCS box demonstrated that loss of this domain resulted in sustained G-CSF-stimulated STAT3 activation, a hypersensitivity of bone marrow-derived cells to G-CSF in proliferation assays and a more severe joint pathology in an acute model of arthritis [27]. This evidence concerns the gene CSF3 and arthritic joint disease.