Consistent with this, higher levels of TNF-α have been found in the CSF of patients with CNS-TB compared with that of healthy controls,[5] and research has shown that the TNF-α to interferon gamma ratio in CSF is highly predictive of IRIS in HIV patients with CNS-TB.[28] Furthermore, thalidomide, a potent TNF-α produced by stimulated monocytes, has been shown to reduce TNF-α levels in the CSF of rabbits with TB meningitis.[29] Therefore, the putative mechanism of action of anti-TNF agents in PR/IRIS would seem straightforward, and reduction of TNF-α levels in the CSF may be expected. The gene discussed is IFNG; the disease is meningeal tuberculosis.