In a similar manner to identifying nonclassical DDR pathway targeting strategies, we recently identified ERK5/MAPK5 through a kinome‐wide RNAi screen as a novel temozolomide resistance factor, with abrogation of ERK5 activity in glioma cells leading to defective DNA repair capacity, likely through inappropriate NHEJ activity prior to mitosis [189]. This evidence concerns the gene MAPK7 and glioma.