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Three mechanisms working in concert, each amplifying the others

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In people with T2DM, GLP-1 analogs have been shown to reduce serum levels of TNF, CRP, and NF-B through the modulation of the protein kinase A-dependent signalling pathway, while lipopolysaccharide (LPS)-induced macrophage activation was attenuated through the same pathways, which led to a reduction in surface expression of CD11b and CD69 and production of IL-4, IL-8, and IL-13 in eosinophils [89]

To put it simply, if a GLP-1 or triple G-agonist even got rid of insulin requirement in 1 out of 10 new onset Type 1 diabetics, that would be a very big deal