MiR-150 inhibits the proliferation and promotes the apoptosis of MCL cells by negatively regulating MET and FOXP1 expression.Premature miR-150 expression severely impairs B-cell development due to a pro- to pre-B-cell transition block, whereas miR-150 deletion promotes B1-cell expansion andincreases antibody production.HGF/MET and FOXP1 signaling pathways are considered as treatment targets for B-cell lymphoma, particularly in MCL. This evidence concerns the gene FOXP1 and mantle cell lymphoma.