Nevertheless, the use of additional genetic brain tumor profiling resources (e.g., longitudinal tumor trajectories [44]) and further experimental validation in diverse genotypic context (IDH1 mutant cell models, etc.)is still needed to clarify whether or how the phenotype of H2AFJ upregulation is linked to a specific clonal or subclonal evolution of a clinically-relevant genotype of brain tumor progression and therapeutic resistance. This evidence concerns the gene IDH1 and brain neoplasm.