Further, in vitro studies using human pluripotent stem cells exposed to activin demonstrated that loss of YAP1 enables differentiation toward anterior primitive streak and endoderm cell fate.[38] There have also been a few prior attempts to generate NF2‐deficient hiPSCs for the purpose of studying tumorigenesis,[39] improving diagnosis of neurofibromatosis type 2,[40] or modeling NF2‐related schwannomas.[41] A preprint by Catasús et al. This evidence concerns the gene NF2 and NF2-related schwannomatosis.