MTOR and legionellosis: Although MTOR is a global metabolic regulator, the potential loss of MTOR-dependent lipogenesis was investigated first because: (1) FBS can compensate for loss of MTOR-driven lipogenesis and when FBS is available cells default to lipid uptake over de novo synthesis to reduce energy expenditure [29]; (2) serum is a major source for cellular lipids and lipid-precursors in vertebrates [29]; (3) rapamycin failed to trigger cell death in Legionella infections and MTOR-driven lipogenesis is insensitive to rapamycin in some cell types [36,60,61].