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The success of first\u2010generation ATP competitive JAK2 inhibitors has validated JAK2 as a therapeutic target, yet clinical benefits remain constrained by issues of off target toxicity, limited mutation allele burden reduction, and the emergence of persistence or resistance. In this review, we focus on a rapidly emerging design paradigm: targeting novel binding sites on JAK2 beyond the canonical ATP pocket\u2014including allosteric sites, covalent anchor residues, and pseudokinase regulatory domains. We summarize structural and computational insights into these new sites, compare mechanistic and therapeutic advantages (such as enhanced selectivity, reduced cross JAK inhibition and potential to overcome resistance) and evaluate preclinical and early clinical evidence. We further identify remaining challenges in the development of next generation JAK2 inhibitors\u2014such as site validation, ligand residence time, covalent binding safety, and rational combination therapies\u2014and propose future directions for translation into the MPN clinic. 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