In contrast, Mφ1 exposed during differentiation to HDAC inhibitors clearly displayed a less pro-inflammatory phenotype, raising the question which HDAC inhibitor-induced cytokine/chemokine profile is optimal for host resistance against Mtb. In line with this, the addition of IFN-γ, a protein known to be vital in TB pathogenesis (70), impaired the effect of HDAC inhibition on bacterial survival in Mφ1. Here, HDAC9 is linked to tuberculosis.