Indeed, dysbiosis can induce tumor-promoting inflammation and genomic instability as demonstrated by Li et al., where increasing secretion of cathepsin K (CTSK) by gut microbiota influenced macrophage polarization into M2 tumor-associated macrophages in colorectal cancer with the increase in IL-4, IL-10 and IL-17 release, leading to a metastatic phenotype [85]. Here, IL17A is linked to neoplasm.