High pPAK1 was observed in NF1-mutant, SUZ12-mutant ST88-14 MPNST cells independent of CRISPRi suppression of NF2 (Supplementary Fig. 9d, e and Supplementary Data 10), suggesting PAK1 activation may be conserved across de-differentiated Schwann cell tumors after loss of either tumor suppressors or epigenetic regulators. The gene discussed is NF1; the disease is neoplasm.