In contrast to p53 stabilization by TRIM25 described in HCT116 cells, complexes between TRIM25, Mdm2, and p53, observed in human lung cancer tissue and lung cancer cells which are characterized by low p53 abundance, indicate that in these cases TRIM25 does rather promote Mdm2-mediated proteasomal degradation of p53 [44]. The gene discussed is TRIM25; the disease is lung cancer.