Therefore, insulin was assessed as well as leptin, glucose, BMI z‐scores and homeostasis model assessment of insulin resistance (HOMA‐IR) levels in children with PWS with respect to nutritional phases relative to two control groups of similar age: healthy‐weight sibling controls (SC) and non‐PWS participants with early‐onset major (clinically severe) obesity (EMO) of unknown etiology. This evidence concerns the gene LEP and Prader-Willi syndrome.