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These findings highlight the critical role of the INS locus in central tolerance and demonstrate that genetic variants can impact both disease risk and progression, underscoring the need to investigate other non-HLA genes associated with T1D

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Structural and pharmacological studies demonstrate that Cagrilintide binds these receptor complexes with high affinity in a manner that resembles endogenous amylin while incorporating modifications that increase peptide stability and prolong receptor engagement [2]

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