Subsequent experiments conducted with three patient-derived GBM cultures, which were varied in terms of EGFR amplification status, additionally elucidated the impact of EGFR amplification on miR-200c/ZEB1 interaction; although miR-200c overexpression exerts an inhibitory effect on ZEB1 regardless of EGFR amplification status, the expression level of ZEB1 was upregulated by miR-200c inhibition only in non-EGFR-amplifying cells, which according to authors may suggest the existence of some additional mechanism affecting ZEB1 in the context of an EGFR amplification environment [43]. This evidence concerns the gene EGFR and glioblastoma.