AKT1 and cancer: The m6A reader, YTHDC2, binds to the insulin‐like growth factor 1 receptor (IGF1R), promotes its translation, and activates IGF1R/Akt/S6 signaling; this leads to radiation resistance.[126] m6A modification confers radiotherapy resistance to bone metastatic prostate cancer (mPCa) cells through the stabilization of enhancer RNA MLXIPe which, through its enhancer activity, promotes oncogenic PSMD9 transcription.[127] m6A modification also confers radiation resistance to cancer cells indirectly via suppression of immune cell infiltration in the tumor microenvironment.