ABSTRACT RNA helicases are a large family of enzymes crucial for virtually all aspects of RNA metabolism, forming the backbone of gene expression regulation. Among them, DEAH‐box helicase 33 (DHX33) has emerged as a pivotal player in fundamental cellular processes, including ribosomal biogenesis, transcription, and translation initiation. A compelling body of evidence now positions DHX33 as a significant oncoprotein, with its overexpression documented in a wide spectrum of human cancers such as lung carcinoma, hepatocellular carcinoma, glioblastoma, and acute myeloid leukemia. Its oncogenic drive is mediated through the transcriptional regulation of genes governing the cell cycle and apoptosis, its interplay with major signaling pathways like Wnt/β‐catenin and PI3K/Akt/mTOR, and its role in metabolic reprogramming, notably the Warburg effect. Furthermore, DHX33 acts as a key downstream effector of potent oncogenes like c‐Myc. Genetic or pharmacological inhibition of DHX33 consistently impedes tumor growth, underscoring its non‐redundant role in oncogenesis. This review systematically synthesizes the current understanding of the mechanisms by which DHX33 promotes t
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