In B-cell lymphoma, resistance to the chimeric anti-CD20 monoclonal antibody rituximab, the first monoclonal antibody to have been registered for the treatment of B-cell lymphomas, is suggested to be due to reduced expression of CD20, the failure of rituximab to trigger the cells leading to inhibition of antibody-dependent and complement-dependent cell toxicity (ADCC and CDC), as well as hyperactivation of antiapoptotic signaling pathways such as p38 MAP kinase, NF-kappaB, ERK1, and AKT [20]. Here, MAPK14 is linked to B-cell non-Hodgkin lymphoma.