This publication describe a human model for Williams syndrome (WS) using iPSC. People affected by WS have a hyper social phenotype but the genes related to this behavior are unknown. We postulated that one of the genes in the WS deletion region, FZD9, could be implicated in the phenotype. Cortical progenitor cells from WS individuals have a high level of apoptosis compared to controls. We showed that FZD9 is responsible for this observation. The progenitor cells that survive form cortical neurons from layer V/VI that are far more complex than controls. WS networks is also more active and with early burst synchronization. We validate these observations by MRI and showed that WS subjects have reduced cortical surface. We also validated the morphometric observations from the iPSC in postmortem tissues. Our data indicates a strong cell autonomous neuronal phenotype that is kept during WS neurodevelopment. This is the first work where iPSC were used to generate insights about a neurodevelopmental disorder and will help us to understand the molecular and cellular basis of the human social brain capacity.