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Conclusion: We identify novel genetic risk variants and complex genetic architecture of cirrhosis and HCC in which metabolic dysfunction is both an independent risk factor and a multiplicative accelerator of disease risk when combined with a high genetic burden or other causes of liver disease

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Oxidative stress, along with PTM of beta-cell proteins, has emerged as a potential mechanism by which the beta-cell becomes immunogenic, effectively marking itself as non-self and triggering an immune response

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