Recent genome-wide association studies have identified more than 100 risk genes for schizophrenia (SCZ) [1]. Many among these are coding for ion channels and ion transporters. While their function has been well characterized, the contributions of common variation in these channels to neurophysiological biomarkers and schizophrenia pathology remain elusive. Here, we explore the effects of altered expression or kinetics of voltage-gated ion channels or calcium transporters on gamma range auditory steady-state (ASSR) deficits, a common biomarker for schizophrenia [2]. We used a network model of coupled excitatory and inhibitory neurons [3], implemented with NetPyNE [4], however using single cell model from a previous studies [5] to implement the genetic variations. We modify the parameters of these single neuron models in a way that mimics the small effects that are expected to be observed in common variants associated with SCZ [6]. Following earlier studies, we included a total of 86 variants of the following genes- CACNA1C, CACNA1D, CACNB2, SCN1A, and HCN1 [6,7]. We then simulated a click train paradigm with stimulation at 40 Hz, to investigate gamma ASSR deficits. Overall, not surprisingly, we found that almost all genetic variants had a small effect on gamma power (72 out of 86 changed gamma power by 15% or less compared to control). However, we also found variants that either strongly reduced or strongly increased gamma power. Interestingly, these were exclusively variants of genes coding for Ca2+ currents. Furthermore, the variants resulting in reduced gamma power also produced a strong, slow oscillatory component in the theta range (4-6Hz). Further analysis revealed that the changes in spectral composition in response to 40Hz stimulation were caused by changes the offset and the slope of parameter ‘m’ of the high-voltage activated Ca2+ channel. Our results deepen the understanding of gamma range ASSR deficits in patients suffering from SCZ and the employed model could ultimately be used in the development of new treatments of the disorder.