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As our understanding of the metabolic-immunological axis in CRC advances, so too will our ability to develop personalized treatment strategies that harness the immune system to combat this disease [79, 80]

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However, Er-targeted therapies are likely to worsen outcomes in carriers of the highly common PNPLA3 p.I148M variant, where ER activation may increase the number of pathogenic malfunctioning defective PNPLA3 enzymes on lipid droplets to drive liver lipid accumulation and worsen MASLD severity (47)