IL1R1 and tuberculosis: As noted by Horne et al.,[15] the SNPs identified as important in PKP3 or TMEMJ16 may be in linkage disequilibrium with SNPs within SIGIRR. The SIGIRR (also known as TIR8) region is a biologically important modulator of TLR-IL-1R signaling, inhibits NF-kappa B, modulates inflammation and in the mouse model has been shown to regulate harmful responses to infections such as TB [16].