In patients with chronic tubulointerstitial nephritis, non-immune metabolic noxae, such as hypokalemia, hyperoxaluria, and hyperuricemia, are involved, along with a medullary ammonia accumulation in the activation of the kidney’s tubular and interstitial cells’ inflammasome complex that induces maturation of pro-inflammatory IL-1β and IL-18 [10]. The gene discussed is IL1B; the disease is hyperuricemia.