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Furthermore, both cell development and the maintenance of different functions require the engagement of GPX4, as its genetic knockout or inactive form of expression leads to embryonic death lethality and subfertility in male mice (Cardoso et al., 2017

By measuring the metabolic flux profile of Mtb in a macrophage model of TB, we discovered that in the absence of Rv1127c, metabolism was dysregulated, and its growth inhibited (Basu et al, 2018)