The higher FcγR-mediated phagocytic pathway activation observed here in the non-IRIS group - including in our ‘baseline-only’ comparison of IRIS- and non-IRIS-group PBMC - therefore suggests a novel, testable hypothesis that a relative deficit in FcγR-mediated phagocytosis occurs in TB-IRIS patient PBMC in vivo, and that this directly affects innate cell-mediated antigen clearance capacity, thereby contributing to higher Mtb antigen loads and aberrant immune responses during TB-IRIS. The gene discussed is FCGR2A; the disease is tuberculosis.