Schizophrenia (SCZ) is a debilitating psychiatric disorder, affecting approximately 1% of the global population. Estimates of the heritability rate of SCZ range around 80%, suggesting a strong genetic component. Loss-of-function mutations in SETD1A have been linked to both SCZ risk and other neurodevelopmental phenotypes. SETD1A is involved in chromatin remodeling through its function as a H3K4 methyltransferase, but how SETD1A loss-of-function mutations lead to altered brain function remains unclear. In the present study, we aim to gain insight into functional consequences of reduced SETD1A function through the neural differentiation of human induced pluripotent stem cells (hiPSCs) carrying SCZ-associated mutations in SETD1A. Genome editing was used to create isogenic hiPSC clones that carry either a frameshift or a splice variant mutation. These lines were differentiated to 2D neural networks and adherent cortical organoids. After differentiation, we noticed a two-fold increase in the number of GAD67-positive interneurons in the SETD1A+/mut neural networks compared to their isogenic controls, relative to the overall number of neurons, in three independently differentiated batches. We also differentiated these SETD1A+/mut hiPSCs and their isogenic controls to adherent cortical organoids (ACOs), which show a semi-3D structure with radial outgrowth and rudimentary cortical layering. In this ACO model, we also observed a two-fold increase in Gad67-positive interneurons, relative to the number of neurons. Taken together, these results could shed light on how SETD1A loss-of-function mutations affects interneurons, and could lead to novel therapeutic strategies.