Despite potential limitations of our non-neural PPD LCL model, the gene networks and DEGs identified (such as GAD1, an indirect indicator of altered GABA release, and UNC13B, a contributor to synaptic vesicle maturation in certain excitatory synapses) tended to functionally correspond to synaptic signaling and neuronal modulation, in support of existing literature linking PPD risk to dysregulated synaptic activity [54,60] (Figure 2D). Here, GAD1 is linked to progressive pseudorheumatoid arthropathy of childhood.