Similar to what was seen in RKIP deficient SIRS splenocytes, inhibiting RKIP using locostatin led to a reduction in IFNγ production significantly after T cell receptors were retriggered with SEA, but were not reduced after restimulation with PMA+ ionomycin, which, again, suggests that downstream of the TCR, RKIP has a role [242]. The gene discussed is IFNG; the disease is systemic inflammatory response syndrome.