Although several studies had already demonstrated that MSCs could be therapeutically effective in this CAC mouse model (Chen et al., 2014; Nasuno et al., 2014; Tang et al., 2015), Chen et al. (2014) found that MSCs inhibited tumor number through IL-6-STAT3 signaling; Tang et al. (2015) showed that MSCs suppressed the development of CAC through regulating the differentiation of Treg cells via Smad2, whereas Nasuno et al. (2014) demonstrated that MSCs inhibited tumor initiation by affecting tumor cell-cycle machinery; however, the protective mechanisms have not been fully defined. The gene discussed is SMAD2; the disease is neoplasm.