Core Viewpoint - The article discusses the discovery of a hyper-translation pathway in monocytes/macrophages that drives cytokine release syndrome (CRS), suggesting that targeting this pathway could be a potential therapeutic strategy for CRS [2][10]. Group 1: Overview of Cytokine Release Syndrome (CRS) - Cytokine release syndrome (CRS), also known as cytokine storm, is a potentially life-threatening inflammatory condition often triggered by infections or immunotherapy [5]. - It is estimated that 50%-90% of patients receiving CAR-T cell therapy experience CRS, with clinical manifestations ranging from mild fever to life-threatening multi-organ failure [5][11]. - The core of CRS pathogenesis lies in the excessive production of pro-inflammatory cytokines, particularly interleukin-6 (IL-6) [5]. Group 2: Mechanisms and Research Findings - The study published in Cell Reports Medicine identifies monocyte/macrophage hyper-translation as a significant feature of CRS pathogenesis [9][11]. - The research team discovered that BCAP is a key regulatory factor for hyper-translation, activating the RSK-EIF4B signaling axis, which leads to excessive translation in macrophages [9][13]. - Genetic deletion of RSK alleviated CRS-related inflammation, and pharmacological inhibition of RSK reduced CRS symptoms in humanized mouse models [9][10]. Group 3: Implications for Treatment - The findings establish hyper-translation as a critical pathogenic feature of CRS and highlight protein translation as a potential druggable target for therapeutic intervention in CRS and other inflammatory diseases [10][13].