Some authors have hypothesized that the delayed onset of weight gain in early infancy observed in PWS may be attributed to the loss of MAGEL2, where its expression may progressively favor the development of leptin insensitivity postnatally, thereby contributing to the obesity phenotype associated with PWS [29, 32], as demonstrated in animal models [39]. The gene discussed is LEP; the disease is obesity due to melanocortin 4 receptor deficiency.