It is obvious that the BM does more than simply supply the GIT with cells of the innate and adaptive immune system. A growing number of studies suggest that BMCs can differentiate into ISEMFs (Lee et al., PLOS ONE 2011;6:e26082) and in the setting of inflammation can be contributors to all lineages of the neovasculature. The role of BMCs in epithelial turnover is more problematic; their contribution after transient mucosal injury seems negligible, but a number of studies in both rodents and man suggest that small numbers of BMCs can be incorporated into the epithelial compartment with more chronic injury (e.g., GvHD in man and chemically induced colitis in rodents); commonly cell fusion seems to be responsible for this. Significantly, this engraftment does not seem to occur in the stem-cell compartment, with the notable single report of the chronically infected murine gastric mucosa, where the BM origin of the stem cells can be the only rational explanation for the complete colonization of the mucosa by BMDCs. In the clinical setting, a role for MSCs in ameliorating colitis seems promising, though the mechanisms by which this is achieved remain somewhat unclear, though both immunomodulatory and regenerative effects of BMCs are likely to be important.