In the chronic low-grade inflammation state characterizing T2D, it can be hypothesized that overexpression of the P2X7R sensitizes pancreatic cells to the elevated levels of eATP, or that the local eATP increase stimulates, via the P2X7R, the NLRP3 inflammasome of infiltrating inflammatory cells to secrete mature IL-1β, and thus, generate a self-amplifying, diabetes-promoting, inflammatory loop in the pancreas [40]. The gene discussed is IL1B; the disease is diabetes mellitus.