Dravet syndrome (DS) is a rare form of epilepsy caused by loss-of-function mutations of the voltage-gated sodium channel NaV1.1. The proposed disease mechanism suggests that these mutations compromise the ability of inhibitory interneurons to regulate network activity, leading to seizure events. However, standard treatments aimed at restoring inhibition have very limited efficacy, suggesting a potential role for excitatory neurons in DS pathogenesis. To explore this, we generated excitatory and inhibitory neurons from control and Dravet hiPSCs and combined them at physiological ratios into in vitro models of cortical circuits. Using these models, we demonstrate hyperactivity of Dravet excitatory neurons. This hyperactivity can be attributed to a greater amplitude of excitatory synaptic inputs received by excitatory neurons. Crucially, this phenotype occurs independently of inhibitory interneurons, suggesting an innate excitatory component in DS. Using mixed genotype co-cultures, we demonstrate that the presence of the NaV1.1 mutation in either the excitatory or the inhibitory component of the network is sufficient to cause network hyperactivity. Recently acquired RNAseq data reveals significant changes, across all Dravet lines, in the expression of ion channels responsible for regulating membrane potential and neuronal excitability. Notably, several of these identified genes have prior genetic associations with similar forms of epilepsy. While the role of these channels is currently being investigated, we believe that these findings present evidence of a central role for excitatory neurons in DS pathogenesis. This previously overlooked excitatory contribution could explain the poor efficacy of current treatments and ultimately facilitate the discovery of novel therapeutical approaches.