The NF2 exon 2–4 region spans the most frequently mutated sites in patients with NF2‐related schwannomatosis (previously known as neurofibromatosis type 2)[11] and deletion of exon 2–3 causes complete loss of Nf2 function and failure of embryogenesis in mice.[3, 10] To examine the role of NF2 during early lineage commitment in hiPSC, we generated NF2 exon 2–4 targeted knockout (NF2−/−) clones from a control wildtype (WT) hiPSC using CRISPR/Cas9. The gene discussed is NF2; the disease is neurofibromatosis.