A new article published in Molecular Cell Research reported that Clostridium difficile infection (CDI) causes nosocomial, antibiotic-associated diarrhea and pseudomembranous colitis, with significant incidence and mortality worldwide. The authors discussed that C. difficile virulence factors are toxin A and toxin B (TcdB) which cause cytopathic or cytotoxic effects and inflammation. This article stated that the available literature are focused on molecular effects of C. difficile toxins (Tcds) on different cells while the status or fate of cells that survived their cytotoxicity remains unexplored. Recently, the susceptibility of enteric glial cells (EGCs) to TcdB cytotoxicity has been demonstrated, however, several EGCs could still survive and were irreversibly cell-cycle arrested and metabolically active, suggesting that EGCs could became senescent. This finding was deemed important and denoted that TcdB induces senescence in EGCs. Experimental evidence further confirmed that TcdB induces senescence in EGCs, as demonstrated by the senescence markers - irreversible cell-cycle arrest, senescence-associated-β galactosidase positivity, flat morphology, early and persistent DNA damage, p27 overexpression, pRB hypophosphorylation, c Myc, cyclin B1, cdc2 and phosphorylated-cdc2 downregulation, Sirtuin 2 and Sirtuin 3 overexpression. Furthermore, TcdB-induced EGC senescence is dependent by JNK and AKT activation, but independent by ROS, p16 and p53/p21 pathways. Therefore, it was concluded that TcdB induces senescence in EGCs. From the results, it was hypothesized that for EGCs that survived TcdB, once they have acquired a senescence state, could cause irritable bowel syndrome (IBS), inflammatory bowel disease (IBD), and tumors due to persistent inflammation, transfer of senescence status, and stimulation of pre-neoplastic cells.