SALL2 is a zinc finger transcription factor with critical roles in development and cancer suppression. During normal development, SALL2 is essential for eye and neural differentiation, with dominant expression in the developing nervous system 1. SALL2 regulates neural differentiation through transcriptional activation of Tuba1a 1 and controls expression of brain-specific transcription factors including SALL3, POU3F2, and NPAS3 2. The gene produces two major protein isoforms (E1 and E1A) with distinct functional roles, with E1A being predominantly expressed across cell types 2. In cancer, SALL2 demonstrates context-dependent functions. It acts as a tumor suppressor in ovarian and colorectal cancers, where SALL2 downregulation promotes cell proliferation, migration, and invasion 34. SALL2 induces p21-mediated cell cycle arrest and activates pro-apoptotic pathways 5. In colorectal cancer, SALL2 negatively regulates Wnt/β-catenin signaling by transcriptionally activating AXIN2 4. Conversely, in glioblastoma, SALL2 is required to reprogram differentiated cells into tumor-propagating stem-like cells 65. SALL2 protein stability is regulated by casein kinase 2-mediated phosphorylation and proteasomal degradation 7. Loss of SALL2 expression is associated with poor survival in multiple cancer types, supporting its potential as a prognostic biomarker 4.