However, no statistically significant difference in sensitivity to GalN/LPS-induced FH was found between Nlrp3-/- mice and the background strain-matched WT mice, as well as between macrophage-depleted mice and vehicle-treated control mice, which could result from a pooled effect of both the diminished beneficial effects and harmful effects upon loss of macrophage or the Nlrp3 gene, or due to the potent toxic effects of GalN/LPS that overwhelm the potential influence of macrophage and NLRP3 on the disease phenotype. The gene discussed is GAL; the disease is familial hyperaldosteronism.