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Langemeijer et al., 2009), suggesting that enhancing residual TET2 activity, or restoring the activity of functionally defective mutant TET2 proteins, could be a particularly viable therapeutic strategy for TET2 deficient hematological malignancies

Our systematic review and meta-analysis showed a dose-response relationship between serum ferritin and dietary iron intake with the incidence of metabolic syndrome and metabolic-associated fatty liver disease(MAFLD), highlighting the importance of iron metabolism in the pathogenesis of these conditions[11]

For example, proteins such as p53, p62, GSK-3, Bif1, Bcl2, Mcl-1, and others regulate both autophagy and apoptosis

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