Background: Slc26a2 is a SO2-4 transporter that is mutated in diastrophic dysplasia. The role of Slc26a2 in several chondrocyte functions is unknown. Results: Slc26a2 is activated by IGF-1 to regulate chondrocyte, proliferation, differentiation, proteoglycan synthesis, and size. Conclusion: Slc26a2 regulates multiple SO2-4-dependent and SO2-4-independent chondrocyte functions. Significance: The findings should help in understanding aberrant SLC26A2 function in diastrophic dysplasia.