FEZF1 is a zinc finger transcription factor with dual roles in neuronal development and cancer biology. In normal physiology, FEZF1 functions as a transcription repressor involved in olfactory sensory neuron (OSN) axonal projection and proper termination [UniProt], contributing to rostro-caudal patterning of the diencephalon and prethalamic formation. FEZF1 mutations cause hypogonadotropic hypogonadism with or without anosmia, with FEZF1 recently added to the genetic screening list for Kallmann syndrome 1. Clinically, dysregulation of FEZF1-AS1, an antisense lncRNA transcript, promotes multiple malignancies. FEZF1-AS1 is upregulated in hepatocellular carcinoma, colorectal cancer, gastric cancer, pancreatic cancer, lung adenocarcinoma, osteosarcoma, and cervical cancer 234. The lncRNA promotes tumorigenesis through competing endogenous RNA mechanisms, sponging tumor-suppressive microRNAs 2. FEZF1-AS1 enhances cancer cell proliferation, migration, invasion, and anti-apoptosis via JAK2/STAT3 signaling, epithelial-mesenchymal transition, and Wnt/β-catenin pathways 53. Additionally, FEZF1-AS1 upregulation promotes TGF-β2-induced lens epithelial cell proliferation and migration 6, relevant to posterior capsule opacification pathology. FEZF1-AS1 represents a potential diagnostic biomarker and therapeutic target across multiple disease contexts.