iNHAs overexpressing CCDC88A-ALK or PPP1CB-ALK were tumorigenic in vivo with 100% penetrance (Fig. 3d, e), forming glial tumors with a high MIB-1 proliferative index, pseudopalisading necrosis, focal GFAP expression, lack of synaptophysin expression and ALK overexpression (Supplementary Fig. 3c, d). The gene discussed is GFAP; the disease is glioma.