Similar observations regarding the regulatory role of BTK on CXCR4 as well as CXCL16, CXCR1, and CXCR2 were found in primary monocytes of XLA patients in which the BTK deficiency may lead to downregulation of these chemokine receptors. This evidence concerns the gene CXCR1 and Bruton-type agammaglobulinemia.