The activity of ILC3s is also influenced by microbial metabolites; in HCC, IL‐17A production by ILC3s was shown to increase in response to dysbiosis marked by reduced Lactobacillus reuteri, whereas acetate supplementation or faecal transplantation suppressed IL‐17A through HDAC inhibition and Sox13 acetylation, delaying tumour progression and sensitising tumours to PD‐1 blockade [136]. This evidence concerns the gene IL17A and neoplasm.