In comparison with primary GBM, secondary GBM had more IDH1/2 and TP53 mutations and CDKN2A loss, a higher frequency of methylated MGMT promoter, and less EGFR amplification, although the number of secondary GBM (n = 3) was limited (Table 3, Figure 1B). The gene discussed is IDH1; the disease is glioblastoma.