| Summary: | Abstract Since the onset of the global pandemic of coronavirus disease 2019 (COVID‐19), there is an urgent need to understand the pathogenesis of the common inflammatory and thrombotic complications associated with this illness leading to multiorgan failure and mortality. It is well established that platelets are hyperactivated during COVID‐19. Data from independent studies reported an angiotensin‐converting enzyme (ACE2)‐dependent severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2) platelet interaction, raising the concern whether ACE2 receptor is the “key receptor” in this process, while other platelet research groups demonstrated that thrombotic events occur via ACE2‐independent mechanisms, where the virus probably uses alternative pathways. In this study, we discuss the conflicting results and highlight the ongoing controversy related to SARS‐CoV‐2‐platelet interaction.
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