Similar to SARS‐CoV, SARS‐CoV‐2 binds to angiotensin‐converting enzyme 2 (ACE2) receptors for entry via endocytosis into alveolar epithelial cells, as well as other cells with ACE2 receptors in the heart, gastrointestinal tract, and kidneys. 2 ,  4  COVID‐19 results from SARS‐CoV‐2 replication, causing early cell death (i.e., apoptosis) and provoking a storm of proinflammatory cytokines (e.g., interleukin‐6 [IL‐6]) disrupting alveolar walls with resulting fluid accumulation in alveoli. 4