protein-like 2 (CNTNAP2) disrupts interneuron migration, results in a loss of interneurons, and mutations in CNTNAP2 are associated with epilepsy and autism in humans (Penagarikano et al., 2011). Calcium/calmodulin-dependent 3′,5′ cyclic nucleotide phosphodiesterase 1A (PDE1A) was recently identified as a marker of a SST neuron subtype (Zeisel et al., 2015). The potassium voltage-gated channel subfamily C member 2 (KCNC2) has been characterized in interneuron function, and may underlie some of the unique intrinsic physiology of these cells (Chow et al., 1999). PHLDA1 was identified as a downstream target of aristalless (ARX), which is itself crucial for interneuron development and migration (Friocourt and Parnavelas, 2011). A specific role for these genes in SST cells will require careful genetic dissection, as past work has shown that genes expressed in multiple subtypes do not necessarily perform similar functions at equivalent stages of maturation, and may depend on combinations of factors within each subtype as they diverge (Batista-Brito et al., 2009; Close et al., 2012). Their precise role will likely need to be determined in a non-human model in order to uncover any specific effects of deletion or overexpression in SST-expressing interneurons. But the fact that mutations in many of these genes have been
