Mechanically, IR induces IRAK1 expression, which was due to direct binding by FOXA2 initiated by IR-elicited STING activation, to suppress autophagic cell death via HECTD3-mediated ubiquitination and degradation of PRDX1, providing a novel mechanism by which IRAK1 overexpression facilitates secondary radioresistance of glioma cells. This evidence concerns the gene IRAK1 and central nervous system cancer.