In line with this interpretation, evidence from complex immune-metabolic diseases indicates that host variants in inflammatory and barrier-related pathways can constrain the range of microbiome configurations that are stably compatible with a given genetic background: in inflammatory bowel disease, genome-microbiome association studies link risk alleles in NOD2, TNFSF15 and IL12B, enriched in innate and JAK-STAT signalling, to characteristic taxonomic shifts and higher dysbiosis indices [58]. The gene discussed is SOAT1; the disease is Other metabolic disease.