MAFF (MAF bZIP transcription factor F) is a basic region leucine zipper transcription factor that functions as both a transcriptional repressor and activator depending on its dimerization partners 1. As a homodimer, MAFF lacks a transactivation domain and acts as a transcriptional repressor 1. However, when forming heterodimers with larger basic-zipper proteins such as NFE2L2/NRF2 or BACH1, MAFF functions as a transcriptional activator, recruiting partners to specific DNA-binding sites 1. In cancer contexts, MAFF exhibits tumor-suppressive properties. In lung adenocarcinoma, MAFF inhibits tumor cell proliferation by regulating SLC7A11, CDK6, and CDKN2C expression, promoting ferroptosis and preventing G1-to-S cell cycle progression 2. Reduced MAFF expression correlates with worse clinical outcomes and cisplatin resistance in lung adenocarcinoma 2. Similarly, in colorectal cancer, MAFF protein is downregulated and reduced expression predicts poor overall and disease-free survival; BAP1-mediated deubiquitination stabilizes MAFF, which suppresses CRC growth through DUSP5/ERK inhibition 3. Conversely, MAFF exhibits context-dependent functions in other disease contexts. In breast cancer, hypoxia-induced MAFF promotes tumor invasion and metastasis through IL11/STAT3 signaling 4. In atherosclerosis, MAFF regulates LDLR expression in a context-dependent manner: positively under non-inflammatory conditions and negatively when complexed with BACH1 during inflammatory stimulation 5. MAFF also participates in Nrf2-dependent oxidative stress responses relevant to acute lung injury 6.