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Agonists like MMF and MK6892, which suppress inflammatory and oxidative pathways upstream of VEGF induction, may complement standard intravitreal anti-VEGF therapies by improving durability, reducing injection burden, and addressing inflammation-driven components of disease that VEGF-neutralization alone does not target

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Fusion of a kinase gene, ALK, to a nucleolar protein gene, NPM, in non-Hodgkin’s lymphoma

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