In cultured keratinocytes pretreated with IFN-γ and TNF-α and stimulated with poly(dA:dT), silencing of CARD18 with small interfering (si)RNA resulted in a significant decrease in AIM2 and CASP1 mRNA expression, however, affected an elevated IL-1β secretion (153), hypothesizing that, in psoriasis, inhibition of IL-1β by CARD18 may entail increased inflammasome priming via a regulatory feedback mechanism. The gene discussed is AIM2; the disease is psoriasis.