Since our previous reports demonstrated that H. pylori-infected p27-deficient mice are susceptible to advanced gastric preneoplastic and neoplastic lesions, [12, 18] we predicted that if gastric cancer originated in bone marrow-derived cells, then wild type mice that received p27-deficent bone marrow cells (group 2) should have the highest cancer incidence of the three experimental mouse groups. This evidence concerns the gene CDKN1B and gastric cancer.