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Thus, CHAC1 serves a dual role: it preserves mitochondrial function by ensuring a cysteine supply under nutrient stress, but it also facilitates ferroptosis by maintaining ETC activity, highlighting its potential as a therapeutic target in cancer treatment (Ward et al., 2024)

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Regarding how HSV-1 reaches the CNS to develop HSE, several routes and mechanisms have been proposed both, as a consequence of primary infection or due to viral reactivations (Figure 1