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Impaired functionality of ISCs in reestablishing the epithelial barrier is a central element in the etiology of IBD, a fact that has been well recognized and extensively studied lately 3,4,5

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Through an m6A-dependent mechanism, METTL16 promotes the expression of BCAT1 and BCAT2, reprogramming BCAA metabolism in AML and contributing to leukemogenesis (Han et al., 2023)