By focusing on normal-weight individuals, our study identified novel loci, such as ARMC6, TMC4, and SUGP2, which were absent in the previous GWAS,24 while corroborating well-established signals at PNPLA3 and TM6SF2. These findings suggest that unique genetic and environmental factors contribute to hepatic steatosis in normal-weight populations, underscoring the importance of targeted GWAS in refining our understanding of the MASLD heterogeneity. This evidence concerns the gene SUGP2 and fatty liver disease.