Korber et al. evaluated a cohort of matched primary and recurrent IDH wild-type gliomas [53], and overall, contrary to the previous report [101], mutational burden was similar in primary and recurrent tumors, and 2/3 of recurrent tumors originated from multiple clones of the primary tumor (oligoclonal origin), while 1/3 were monoclonal. Here, IDH2 is linked to neoplasm.