This critical role in deciding the fate of an infection is exemplified in viral diseases such as COVID‐19, where the timely activation of TLRs (e.g., TLR3 and TLR7) is essential for a protective antiviral response, while the dysregulated hyperactivation of others (e.g., TLR2 and TLR4) can trigger a pathological “cytokine storm,” leading to severe immunopathology and acute respiratory distress syndrome (ARDS) [8, 12]. This evidence concerns the gene TLR7 and COVID-19.