There is strong evidence supporting the association between nonalcoholic fatty liver disease and fructose consumption.1 Fructose particularly drives hepatic de novo lipogenesis (DNL), which promotes lipotoxicity and steatohepatitis. Schwarz et al2 have recently shown that isocaloric fructose restriction is associated with a reduction in liver fat and DNL in obese children. We note with interest the marked heterogeneity in participant responses to the low-fructose diet, with a significant proportion of participants exhibiting minimal or no change from baseline liver fat and DNL, despite achieving overall statistical significance.