However, those DP mice exhibited a declined endocrine level of leptin, which was the presumed cause of obesity in patient with DF of 16p11.2.[14] Supporting this, other two similar mouse models with engineered 7Slx1b‐Sept1 or Coro1a‐Spn region obtained a small body size in DF mice, although the weight status of the DP mice was not mentioned.[11, 12] Thus far, DP mice seem to be suitable models for investigating the role of 16p11.2 rearrangement in obesity genesis, which eclipses clinical case studies where heterogeneity is very high. This evidence concerns the gene LEP and Obesity.