The INGs function as type II tumor suppressors, being frequently down-regulated or mislocalized in different tumor types [34]–[37], and murine knockout models of ING1 show development of B cell lymphoma independent of p53 status [38], although ING1 protein can increase p53 levels through effects upon p53 polyubiquitination [39]. The gene discussed is TP53; the disease is B-cell non-Hodgkin lymphoma.