Surprisingly, the SARS-CoV-2 virus inhibits STAT-1 and IFN function, leading to the compensatory activation of STAT3, which would be responsible for some phenomena of severe COVID-19, such as coagulopathy, thrombosis, proinflammatory state, T-cell lymphopenia, increased ACE2 expression (STAT-3 alpha), and also increased procalcitonin, which could falsely be interpreted as bacterial superinfection [28]. The gene discussed is IFNA1; the disease is COVID-19.