eATP can act as a second signal that activates inflammasomes, as shown by the observation that exposure to CoV-2 S followed by eATP triggered a stronger expression of pro-IL-1β, ASC, NLRP3 and gasdermin D in macrophages derived from COVID-19 patients than in SARS-CoV-2 naïve cells, and only patient-derived macrophages exhibited active ASC specks and increased secretion of TNF-α and IL-1β (229). The gene discussed is IL1B; the disease is COVID-19.