Moreover, it was shown that increased release of TNFR due to ADAM17 activation by mannose-capped lipoarabinomannan facilitates the maintenance of Mycobacterium tuberculosis infection [27], and that myeloid ADAM17-deficiency leads to a reduced bacterial burden in the inflamed lung upon sepsis caused by Gram-negative bacteria [28,29]. The gene discussed is ADAM17; the disease is Sepsis.