,93,94 These findings highlight the critical role of CXCL9–11 during early Mtb infection (before immune priming), where they promote the recruitment of lymphocyte populations (CXCR3+ T cells); however, overexpression may drive TB sequelae via pro-inflammatory myeloid-T, NK cell circuits, which potentiate pro-inflammatory response mechanisms and bacterial dissemination.91 The gene discussed is CXCR3; the disease is tuberculosis.