According to some studies, inducing necrosis and apoptosis or reactivating TB, especially in immunocompromised patients, can lead to an increase in interleukin (IL)-17 and tumor necrosis factor (TNF)-α, which can either decrease tumor protein 53 (TP53) activity or increase B-cell lymphoma 2 (Bcl-2) expression, decrease (Bcl-2-associated X protein) Bax expression, and inhibit caspase-3 expression by reducing mitochondrial cytochrome oxidase expression [40,41]. Here, TNF is linked to tuberculosis.