BLCAP (BLCAP apoptosis inducing factor) functions as a tumor suppressor gene that regulates cell proliferation and apoptosis through multiple mechanisms. The protein induces S-phase cell cycle arrest and apoptosis via RB1-dependent pathways that are independent of p53 and NF-κB signaling 1. BLCAP directly interacts with RB1 and inhibits its phosphorylation, preventing G1/S checkpoint progression and maintaining cell cycle control 2. The gene modulates expression of proliferation, cell cycle, and apoptosis-related genes, including upregulation of p21(WAF1/CIP1) and downregulation of anti-apoptotic proteins Bcl-XL and Bcl-2 1. BLCAP undergoes extensive A-to-I RNA editing by ADAR1 and ADAR2 enzymes, creating alternative protein isoforms 3. Importantly, RNA editing levels are generally decreased in multiple cancers including astrocytomas, bladder, and colorectal cancers compared to normal tissues 3. Over-editing of BLCAP promotes its degradation through ubiquitination, reducing its tumor suppressor function and facilitating increased cell proliferation and reduced apoptosis 4. In hepatocellular carcinoma, BLCAP over-editing activates the AKT/mTOR signaling pathway, contributing to tumorigenesis 5. The protein shows promise as both a therapeutic target and potential biomarker for immunotherapy response 6.