In hepatocellullar carcinoma cells, silencing of LRF/ZBTB7A increased p53 expression and initiated caspase-dependent apoptosis via death receptor- and mitochondria-mediated pathways [37], whereas in breast cancer, LRF/ZBTB7A anti-apoptotic function involved Survivin, a negative regulator of apoptosis [52], discussed in a separate section of this review. This evidence concerns the gene ZBTB7A and breast carcinoma.