Therefore, we hypothesized that KIR2DL1/HLA-C group C2 interactions would confer strong inhibitory responses [74,75], at least in those individuals with critical COVID-19 from our cohort that were homozygous for HLA-C group C2 alleles and of whom we previously described that they show an impaired cytotoxic response against SARS-CoV-2 mostly based on high levels of NK, NKT, and CD8+ T cells that display immune exhaustion markers and poor cytotoxic functionality [8]. The gene discussed is KIR2DL1; the disease is COVID-19.