It was shown that diverse growth-limiting stresses, such as hypoxia, low pH or Fe, activated tgs1-mediated triglyceride synthesis and accumulation by directing acetyl-CoA away from the tricarboxylic acid cycle, which led to decreases in the growth and antibiotic efficacy in Mycobacterium tuberculosis, and that both the overexpression of citA and deletion of tgs1, which disrupted the metabolic switch, contributed to the bacterial growth responding to stress and caused antibiotic sensitivity during infection [10]. This evidence concerns the gene TGS1 and infection.