Hypothetic model on how the pro-inflammatory CNF1 activity can be connected to cancer. CNF1-dependent Rho activation stimulates NF-κB nuclear translocation and trans-activation, through the classical Akt/IKK-mediated pathway. NF-κB induces the transcription of genes coding for proteins involved in inflammation and apoptosis, that is the pro-inflammatory molecules IL-6, IL-8, TNF-α and Cox-2, and anti-apoptotic factors, such as Bcl-2. This last also causes elongation and enrichment of the mitochondrial network, an aspect somehow linked to transformation. On the other hand, by mean of its activity on the actin cytoskeleton organization, CNF1 is able to provoke cell junctions disruption and to strongly enhance cellular motility, a phenomenon strictly linked to invasiveness and metastasis.