FOSL2 is a transcription factor subunit of the AP-1 complex that regulates diverse cellular processes across multiple pathological contexts. As a component of AP-1, FOSL2 functions as a sequence-specific DNA-binding transcription activator 1. In immune contexts, FOSL2 serves as a key determinant of Th17 cell plasticity within the global transcriptional regulatory network governing Th17 differentiation 1. In cancer biology, FOSL2 demonstrates multifaceted roles: it activates Wnt5a transcription in breast cancer-associated fibroblasts to promote VEGF-independent angiogenesis 2, regulates EFNA1 through super-enhancer-driven mechanisms to fuel cervical cancer progression via the Src/AKT/STAT3 pathway 3, and participates in glioblastoma evolution by coordinating tumor-macrophage interactions through the HIF1A-FOSL2 and FOSL2-ANXA1-FPR1/3 axes 4. In cisplatin-resistant non-small cell lung cancer, FOSL2 activates NAMPT expression to suppress ferroptosis 5. FOSL2 expression is also dysregulated in osteoarthritis cartilage, where it represents a therapeutic target mediating abnormal gene expression 6. Additionally, FOSL2 exhibits differential chr2 accessibility in monocyte-derived versus tissue-resident alveolar macrophages in idiopathic pulmonary fibrosis 7, and EP300-mediated acetylation of FOSL2 accelerates cervical cancer proliferation 8. These findings establish FOSL2 as a context-dependent transcriptional regulator with significant implications for cancer progression, inflammatory diseases, and fibrotic pathologies.