EGFR and neoplasm: Jutten et al. found that autophagy activity influenced the expression of EGFR and the resistance to EGFR-targeting therapies could be reduced by downregulating autophagy [47, 48]; IL-17 (interleukin-17), as a signature proinflammatory cytokine of the CD4+ T helper 17 (Th17) cells [49], was shown to participate in the formation and advancement of various tumours [50] and was widely distributed in the tumour microenvironment, where it has twin roles in tumourigenesis and tumour suppression [51].