SALL4 is a zinc finger transcription factor that functions as a member of the spalt-like family of developmental genes 1. In normal development, SALL4 plays a critical role in maintaining embryonic and hematopoietic stem cell self-renewal and pluripotency through interaction with developmental regulators like OCT4 and NANOG 2. SALL4 expression normally decreases during development and is absent in most differentiated adult tissues 3. Heterozygous SALL4 mutations cause Duane-Radial Ray syndrome and related developmental syndromes characterized by limb malformations, ocular defects, and congenital heart disease 1. Notably, thalidomide induces SALL4 degradation exclusively in humans, primates, and rabbits, mechanistically explaining thalidomide's species-specific teratogenicity and producing phenotypes that mimic SALL4 loss-of-function mutations 1. In cancer, SALL4 becomes aberrantly reactivated and acts as an oncofetal gene 4. SALL4 expression is detected in ~86% of breast cancers and various other malignancies 2. SALL4 positivity significantly increases overall mortality (HR=1.4) and disease recurrence (HR=1.52) across multiple cancer types 4. SALL4 regulates cancer cell proliferation, apoptosis, metastasis, and drug resistance through epigenetic modulation as a transcriptional activator or repressor 3. In myelodysplastic syndrome, hypomethylating agent treatment can paradoxically demethylate SALL4 promoter regions and upregulate SALL4 expression in 30-40% of patients, associated with worse outcomes 5. SALL4 overexpression predicts relapse in acute lymphoblastic leukemia with 92.3% sensitivity 6, establishing SALL4 as a promising diagnostic, prognostic biomarker, and therapeutic target.