The cytokine storm in cervical cancer induces a series of molecular and cellular responses, including the activation of key signaling pathways such as Janus kinase/signal transducer and activator of transcription (JAK/STAT), nuclear factor-kappa B (NF-κB), and mitogen-activated protein kinase (MAPK), that drive tumor cell survival, proliferation, and invasiveness. The gene discussed is SOAT1; the disease is neoplasm.