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Nonalcoholic fatty liver disease (NAFLD) has recently become an emerging health problem worldwide (1). The pathogenetic mechanisms involved in the development and progression of NAFLD are due to genetic predisposition that expresses a metabolic profile associated with high energy food intake (2). The most accurate estimate of the worldwide prevalence of NAFLD is 24–25％ of the general population, and ranges from 5–18％ in Asia to 20–30％ in the Weste countries (1,3). Nowadays, the reason for this variability is not clear yet. However, it is plausible that genetic factors could play a major role in pathogenesis and the advances in genomics, transcriptomics, and proteomics have highlighted new pathogenic pathways. In fact, increasing literature data support the role of single nucleotide polymorphisms (SNPs), and in particular the SNPs of genes involved in insulin signaling, lipid homeostasis, and oxidative stress, not only in the susceptibility to develop NAFLD, but also in the severity of liver damage and in the etiology of multisystemic metabolic disorders (4). The development of the Genome Wide Association Study technology has allowed the identification of many SNPs involved in the onset of NAFLD, since they can change the stages of development, the rate of progression, and the efficacy of treatment (5). Recently, Tricò et al. investigate the clinical and genetic features associated with pediatric NAFLD in a prospective study in a large multiethnic cohort of obese adolescents (6). A total of 503 subjects, identified as "The Yale Pediatric NAFLD cohort", were enrolled, including 191 (38.0％) Caucasians, 134 (26.6％) African Americans, and 178 (35.4％) Hispanics.