cell lines) in where transforming mutations are already present could prevent studies on the role that specific mutations might play during gliomagenesis. Directly addressing the lack of model for studying driver mutations, the Tabar laboratory first reported on the use of NPCs differentiated from human ESCs for studying the role that histone 3.3 mutations play in the formation of pediatric gliomas2. Along a similar line, our own results demonstrate the suitability of hiPSCs technologies for the establishment of GTIC-like models recapitulating features observed in adult human gliomas.
