This homing defect is consistent with findings in the mouse model, in which MST1 deficiency leads to naive T-cell lymphopenia and an impaired egress of mature T lymphocytes from the thymus to secondary lymphoid organs, associated with an impaired chemotactic response to several chemokines, including the CCR7 ligands CCL19 and CCL21 [32], [33]. This evidence concerns the gene CCL21 and lymphopenia.