YTHDF2 promotes ATP synthesis and immune evasion in B cell malignancies YTHDF2 modulates oncogenic transformation and immune evasion across multiple B cell cancers by stabilizing m5C-modified mRNAs and destabilizing m6A-modified mRNAs, thereby serving as a dual reader for both m5C and m6A modifications. Small molecules that target YTHDF2 reduce ATP synthesis and are therapeutic candidates for B cell malignancies, especially when combined with CAR-T therapy or bispecific engagers.

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