PCSK7’s dual roles in metabolic regulation and immune modulation suggest precision therapeutic strategies—hepatocyte-targeted ASO agents suppressing its pro-lipogenic function have alleviated NAFLD phenotypes in murine models, potentially extendable to metabolism-associated CRC subtypes, while PCSK7 inhibitors synergizing with anti-PD-1 therapy reversed T-cell exhaustion in colon cancer organoids. This evidence concerns the gene PCSK7 and metabolic dysfunction-associated steatotic liver disease.