Results showed that systemic TNF and IFN-γ levels in patients are helpful in dividing patients into those who have an excessive response to cytokine and cytotoxic molecule production (TNFHIFNγH) and those who have less ability to activate said response (TNFN-LIFNγN-L), suggesting that the pathophysiology of critical COVID-19 can be mediated in different pathways. This evidence concerns the gene TNF and COVID-19.