Increasing rates of interleukin (IL)-17 and tumor necrosis factor alpha (TNF-α) as a result of necrosis, apoptosis or TB reactivation, will either decrease P53 activity or increase the expression of B-cell lymphoma-2 (Bcl-2), decrease Bax-T, and cause the inhibition of caspase-3 expression due to decreasing the expression of mitochondria cytochrome oxidase. Here, BAX is linked to tuberculosis.