IL17A and tuberculosis: Many studies reported that the induction of necrosis and apoptosis or TB reactivation might result in increasing TNF-α and IL-17 that will either decreases the activity of P53 or increase the BCL-2 expression, decrease Bax-T, and cause the inhibition of caspase-3 expression due to decreasing the expression of mitochondria cytochrome oxidase (Mariani et al., 2001; Liuzzo et al., 2013).