Consistent with the above observations, we have previously shown that FOXG1 physically and functionally interacts with TLE proteins in GBM patient‐derived BTICs, and that TLE knockdown, as well as overexpression of the TLE antagonist GRG6, mimics the effects of FOXG1 attenuation in these cells (Verginelli et al., 2013). Here, FOXG1 is linked to glioblastoma.