In the TGF‐β‐rich microenvironment, such as in the intestines, tumour or damaged tissues undergoing regeneration and remodelling, the persistence of pathogen or autoantigen may activate monocytes and dendritic cells, and thereby repress Foxp3 transcription and promote Th17 differentiation, as observed in rheumatoid arthritis patients 77. This evidence concerns the gene TGFB1 and neoplasm.