Expression of Hk2 was 1.6-fold higher in uninfected Sirt3−/− BMDM compared to WT (Fig. 4C) and was not further increased by M. tuberculosis, suggesting that the infection-induced increase of Hk2 in WT macrophages resulted from SIRT3 downregulation (Fig. 4C). This evidence concerns the gene HK2 and infection.