To validate experimentally the role of TEAD1 in GBM migration, we generated stable population knockout of TEAD1, and its better studied paralog TEAD4, in patient-derived, low-passaged GBM cells, by using CRISPR-Cas9 genome editing to introduce loss-of-function mutations (Fig. 3a, Supplementary Fig. 5a–b). Here, TEAD4 is linked to glioblastoma.