To address this gap, our review synthesizes extant literature to (1) examine theoretical and empirical evidence linking chronic stress to disruptions in GR and NF‐κB associated pathways; (2) characterized GR modifications (including posttranslational changes and epigenetic regulation) and mechanisms underlying GR resistance under chronic stress; and (3) elucidate how the altered GR‐NF‐κB axis can promote tumor initiation, progression, and resistance to therapy. This evidence concerns the gene NR3C1 and neoplasm.