Loss of BAX also renders colorectal cancer cells resistant to TRAIL/Apo2L-mediated radiosensitization. These same v-BCL-2 proteins cooperate with loss of retinoblastoma protein and p53 tumor suppressor function, by inactivating the BAX and BAK apoptotic pathway to promote epithelial solid tumor growth and resistance to chemotherapy. This is in clear contrast to other carcinomas where BAX is frequently inactivated which correlates to a poor prognosis . There were no significant differences of the BAX levels between goitres or the adenomas.