Debatably more dramatic than altering neutrophil metabolism, Isoniazid treatment of TB-infected mice has been shown to drive apoptosis of activated T cells in vivo which, while promoting clearance of TB infection, supresses host immunity and inflammatory cytokine production acutely, enhancing the overall chance of reinfection.62 The significant loss of T-cell-associated cytokines, TNFα, IL-17, and IL-9 with Isoniazid treatment, suggests that the reduced inflammatory state of the TNFΔARE mice may be attributed to such mycobacterial-independent mechanisms although require future validation. This evidence concerns the gene IL17A and tuberculosis.