Importantly, as blockade of Gal1 in most cancer models results in CD8+ T-cell-mediated tumor rejection,32, 33 it seems apparent that under conditions in which Gal1 secretion is substantially increased (i.e., tumor or inflammatory microenvironments), contraction of the CD8+ T-cell compartment and inhibition of CTL function will certainly prevail. The gene discussed is CD8A; the disease is neoplasm.