IL-17 promotes tumor invasion by increasing MMP-9 expression and VEGF-dependent angiogenesis,19 which is counterbalanced by the recruitment of CD16+ neutrophils and antigen-specific CTLs to the tumor tissues.21 This dual role of IL-17A in the microenvironment of CRC is not completely understood and maybe highly dynamic depending on the state of the adaptive immune system.34 For instance, we observed significantly higher levels of TNFSF11 (RANKL), CCR6 and CCL20 in the IL-17Ahigh versus IL-17Alow groups. This evidence concerns the gene TNFSF11 and neoplasm.