In addition to inhibiting TMPRSS2‐mediated S2' priming by LL‐37, we speculate that the basal levels of LL‐37, especially its levels in macrophages, might be vital for orchestrating the immune response to SARS‐CoV‐2 infection, and these patients with deficient levels of LL‐37 seem more prone to developing into a severe condition manifested as hyperinflammatory responses and immune dysfunction. This evidence concerns the gene CAMP and immune system disorder.