Neurodevelopment is a finely orchestrated process marked by the sequential, but intimately connected events of synapse formation, maturation, and the critical GABA shift, where GABAergic neurotransmission transitions from excitatory to inhibitory. The precise timing and intricate balance of excitatory and inhibitory signaling is crucial for establishing functional neural circuits, and when disrupted contribute to neurodevelopmental disorders (NDDs) like autism spectrum disorder (ASD) and epilepsy. Exploring human aspects of neuronal development and functioning face challenges due to limitations of model organisms and earlier in vitro models. Here, we employed improved methodologies to generate mature glutamatergic and GABAergic neurons and functional networks from human induced pluripotent stem cells (hiPSCs). Through a multidisciplinary hiPSC-phenotyping platform, combining protein profiling, microelectrode array (MEA) neuronal network measurements, and transcriptomics, we demonstrate reliable modeling of intricate synaptic networks and recapitulation of critical neurodevelopmental events in vitro, crucial for deciphering the molecular underpinnings of NDDs. Utilizing patient-specific iPSCs, we set out to uncover whether a delayed GABA shift and disrupted synaptic connectivity, converge as key mechanisms driving the prevalent excitation/inhibition (E/I) imbalance in ASD. Remarkably, patient iPSC-derived neurons carrying SCN1A mutations revealed a delayed GABA shift and altered network activity, with varying degrees of severity mirroring the clinical phenotypes. Uncovering convergence of ASD-linked genes at the molecular level will guide targeted investigation into the precise mechanisms underlying patient-specific developmental network MEA fingerprints, laying the groundwork for personalized therapeutic interventions, tailored to distinct developmental periods.