may underlie the observed size reduction of patient-derived neurospheres and the decreased neural differentiation efficiency in patient-derived neurospheres. In support of this theory, abnormal neurogenic-to-gliogenic transition competence balance in patient-derived differentiated cells could be partially recovered by the addition of p38 inhibitor. The recent studies reported that the RAF/MEK/ERK pathway also controls gliogenesis.47 In the patient-derived neurospheres, upregulated genes were significantly enriched for ERK-mediated nuclear events in addition to MAPK-associated pathways (Supplementary Table 6), implying the involvement of the ERK pathway in the abnormal of neurogenic-to-gliogenic transition competence balance in the patient-derived neurospheres seen in our study.
