COVID-19 began as a pneumonia outbreak in Wuhan, China, in 2019 and then it spread globally. SARS-CoV-2 virus possesses a receptor binding region which can bind to angiotensin converting enzyme 2 receptors of the host cells, allowing the virus to infect host cells. COVID-19 illness can range from normal cough and cold to life-threatening acute respiratory distress syndrome and multiorgan failure. Immune dysfunction and cytokine dysregulation, known as “cytokine storm syndrome,” play a crucial role in progressing from mild to severe disease. In COVID-19 patients, elevation of cytokines and interferons is prevalent in SARS-CoV2-induced pneumonia, resulting in a cytokine storm syndrome. Identifying authorized medicines with appropriate safety profiles is crucial for treating hyperinflammation. Although some aspects of this topic have been explored previously, a thorough understanding of COVID cytokine storm (COVID-CS) is extremely necessary. In this chapter, we describe an updated and comprehensive picture of COVID-CS. Here, we reviewed the immunopathological aspects of COVID-CS, including its mechanism of action, the role of innate and adaptive immune responses, the individual cytokines and their associated signaling pathways involved in COVID-CS.