The overall goal of Michael Higley’s project was to elucidate the changes in synaptic connectivity caused by interneuron-specific loss of the autism-associated gene tuberous sclerosis complex 1 (TSC1). Higley and his group used electrophysiological analyses to reveal that deletion of TSC1 from a subclass of GABAergic interneurons that express the marker parvalbumin produces an increase in synaptic inhibition onto nearby excitatory pyramidal neurons. This result is surprising, as previous studies found that global deletion of TSC1 resulted in weakened inhibition and hyperexcitability in the network¹,². Higley’s findings illustrate that dysfunction of autism-linked genes can produce complex and competing outcomes depending on the identity of neurons affected.