There is a key role for the mSCN, recruited from the bone marrow into the tumour microenvironment, in cancer growth and progression to metastasis [12,15,16,17]; for example, when chronic gastritis, metaplasia and dysplasia were induced by Helicobacter felis infection, or by constitutive expression of IL-1β in the stomach of αSMA-RFP+ transgenic mice (in which expression of RFP was regulated by the αSMA promoter), increased numbers of αSMA positive cells (myofibroblast cells) were observed in both mouse models at the later stage of dysplasia [12]. This evidence concerns the gene ACTA1 and neoplasm.