For example, NLRP6 was reported to control epithelial self-renewal and microbiota homoeostasis to protect against inflammation-induced tumour development in the intestine44–46, although the finding that NLRP6 exacerbated graft-versus-host disease, which was independent of microbiome change, was in contrast to the protective role of NLRP6 in tumorigenesis47. The gene discussed is NLRP6; the disease is neoplasm.