In keeping with the shift of glucose to lipid metabolism when the capacity of GK for hepatic glycogen synthesis is exceeded [15, 47], we found genetically-proxied impaired GK-GKRP interaction causally increased plasma TG, LDL-C, ApoB levels, decreased HDL-C level as well as increased risks of MASLD and CAD. This evidence concerns the gene APOB and metabolic dysfunction-associated steatotic liver disease.