Consistent with the genome-wide association study, silencing MBOAT7 by an antisense oligonucleotide, which resulted in lower MBOAT7 expression primarily in liver, adipose tissue, and cells within the reticuloendothelial system, caused a nonalcoholic fatty liver disease phenotype in fat-fed mice (7). Here, MBOAT7 is linked to metabolic dysfunction-associated steatotic liver disease.