Reciprocal effects on neurocognitive and metabolic phenotypes in mouse models of 16p11.2 deletion and duplication syndromes.

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This study shows that for families affected by proximal 16p11.2 deletions or duplications (BP4–BP5), having one copy missing or extra can lead to opposite patterns in learning, behavior, and growth, helping families understand why children may show very different challenges (such as activity level, memory, or weight) depending on the type of 16p11.2 change and reinforcing the importance of individualized care rather than one‑size‑fits‑all expectations.