CLK2 and neoplasm: TCGA transcriptome analysis of 16 different cancer types indicated a global increase in IR levels in cancerous tissues, compared to the matched normal tissues.[11] The increase of IR may contribute to tumor progression by inactivating tumor suppressor genes or generating novel tumor neoepitopes.[2] The IR pattern was not examined in glioma likely due to the lack of the matched normal and cancer samples in the TCGA cohorts.[11] By utilizing the GSC differentiation model, our findings suggest that the CLK2 condensates‐mediated IR suppresses glioma progression.