Results provided in this work showed that (1) the inflammasome proteins are particularly overexpressed in critically ill patients with COVID-19, (2) SARS-CoV-2 enhances inflammasome proteins and inflammation through TLR2 activation, (3) NAC is able to inhibit inflammasome activation in cells stimulated with SARS-CoV-2 proteins through the inhibition of Nf-κB and NLRP3. The gene discussed is NFKB1; the disease is COVID-19.