SLITRK6 is a leucine-rich repeat transmembrane protein that functions as a regulator of neurite outgrowth essential for normal sensory development 1. Primary Function: SLITRK6 regulates synapse assembly and axonogenesis during neurodevelopment, with particular importance in the developing retina and inner ear 1. Mechanism: The protein localizes to the cell surface and plasma membrane where it promotes synaptogenesis 1. Loss-of-function mutations impair cell surface localization, resulting in delayed retinal synaptogenesis and increased axial eye length 1. Disease Relevance: Autosomal-recessive SLITRK6 mutations cause a syndromic form of deafness and myopia characterized by high myopia and sensorineural hearing loss 12. Additionally, congenital cytomegalovirus infection downregulates SLITRK6 expression through viral IE2 proteins, potentially contributing to infection-associated sensorineural hearing loss 3. Clinical Significance: Beyond sensory disorders, SLITRK6 has emerged as a therapeutic target in cancer. The protein is upregulated in urothelial carcinoma—particularly upper tract urothelial carcinoma—where it promotes cell proliferation via PI3K/AKT/mTOR signaling and the Warburg effect 45. Antibody-drug conjugates targeting SLITRK6 have received FDA breakthrough designations for advanced urothelial carcinoma 6.