In TMEV murine MS model, loss of galectin-3 (Gal-3) inhibited an increase in chemokine levels, reduced immune cell migration into SVZ, restored SVZ proliferation, and increased the number of progenitors in the corpus callosum, thereby modulating the SVZ neurogenic niche's response to MS [302]. The gene discussed is LGALS3; the disease is myeloid sarcoma.