SPN and obesity disorder: 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.