Structural changes in the gut microbial community have been shown to accompany the progressive development of colorectal cancer.In this review we discuss recent hypotheses on the mechanisms involved in the bacteria-mediated carcinogenesis,as well as the triggering factors favoring the shift of the gut microbiota from a mutualistic to a pro-carcinogenic configuration.The possible role of inflammation,bacterial toxins and toxic microbiota metabolites in colorectal cancer onset is specifically discussed.On the other hand,the strategic role of inflammation as the keystone factor in driving microbiota to become carcinogenic is suggested.As a common outcome of different environmental and endogenous triggers,such as diet,aging,pathogen infection or genetic predisposition,inflammation can compromise the microbiota-host mutualism,forcing the increase of pathobionts at the expense of health-promoting groups,and allowing the microbiota to acquire an overall pro-inflammatory configuration.Consolidating inflammation in the gut,and favoring the bloom of toxigenic bacterial drivers,these changes in the gut microbial ecosystem have been suggested as pivotal in promoting carcinogenesis.In this context,it will become of primary importance to implement dietary or probiotics-based interventions aimed at preserving the microbiota-host mutualism along aging,counteracting deviations that favor a pro-carcinogenic microbiota asset. Structural changes in the gut microbial community have been shown to accompany the progressive development of colorectal cancer. This review we discuss recent hypotheses on the mechanisms involved in the bacteria-mediated carcinogenesis, as well as the triggering factors favoring the shift of the gut microbiota from a mutualistic to a pro-carcinogenic configuration. The possible role of inflammation, bacterial toxins and toxic microbiota metabolites in colorectal cancer onset is specifically discussed. On the other hand, the strategic role of inflammation as the keystone factor in driving microbiota to become carcinogenic is suggested. As a common outcome of different environmental and endogenous triggers, such as diet, aging, pathogen infection or genetic predisposition, inflammation can compromise the microbiota-host mutualism, forcing the increase of pathobionts at the expense of health-promoting groups, and allowing the microbiota to acquire an overall pro-inflammatory configuration. Consolidolid ating inflammation in the gut, and favoring the bloom of toxigenic bacterial drivers, these changes in the gut microbial ecosystem have been suggested as pivotal in promoting carcinogenesis. In this context, it will become primary importance to implement dietary or probiotics-based interventions at preserving the microbiota-host mutualism along aging, counteracting deviations that favor a pro-carcinogenic microbiota asset.