Although novel severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2)‐mediated pulmonary inflammation has recently attracted great attention, its pathology and pathogenesis are not clear. Notably, due to both its high infective and pathogenicity, SARS‐CoV‐2 infection may cause a severe sometimes fatal respiratory disease. A specific vaccine, which relies on the analysis of SARS‐CoV‐2 structural protein‐derived antigenic peptides, is indispensable for restraining the spread and reducing the mortality of SARS‐CoV‐2. SARS‐CoV‐2 infections activate cytototxic, myeloid‐derived suppressor cells, dendritic cells, macrophages, as well as natural killer, B, helper T, and regulatory T cells, thus further stimulating innate and antigen‐specific immune responses. Nevertheless, many immune effector cells cause hyperinflammation and pulmonary immunopathology by releasing proinflammatory cytokines and chemokines, including interferon (IFN)‐α, IFN‐β, IFN‐γ, monocyte chemoattractant protein‐1, macrophage inflammatory protein (MIP)‐1A, MIP1B, interleukin (IL)‐1, IL‐2, IL‐4, IL‐6, IL‐7, IL‐8, IL‐9, IL‐12, IL‐17, and IL‐18, platelet‐derived growth factor, fibroblast growth factor, tumor necrosis factor‐α, and induced protein 10. Interestingly, related products derived from SARS‐CoV‐2 are likely to trigger immune evasion. Therefore, investigating SARS‐CoV‐2‐specific vaccines, blocking immunopathology, and prohibiting immune evasion are urgently required for treating SARS‐CoV‐2 infection. In this review, we emphatically illuminated the development of a SARS‐CoV‐2‐specific vaccine based on the analysis of epitopes, also expounding the molecular mechanisms of SARS‐CoV‐2‐mediated cytokine release syndrome. Furthermore, we comprehensively discussed SARS‐CoV‐2‐associated immune evasion and lung immunopathology. Lastly, potential therapeutic strategies against SARS‐CoV‐2 were explored.