It was recently shown that high levels of c-Myc caused by the constitutive activity of EGFRvIII, a mutated form of EGFR, amplifies the transcription of hnRNPA1 in GBM and the alternative splicing of Max into its C-terminally truncated ΔMax isoform [11]. This evidence concerns the gene HNRNPA1 and glioblastoma.