For the same, we used 2-ME, a metabolite of 17-β estradiol that inhibits the nuclear accumulation and transcriptional activity of HIF-1α, as a tool to explore HIF-1α-mediated activation of the NF-κB signaling pathway in PBMCs isolated from patients with active TB and individuals with LTBI [20]. The gene discussed is HIF1A; the disease is tuberculosis.