Mathieu et al. showed that decreasing Gal-1 expression in B16F10 mouse melanoma cells via siRNA sensitized cells to the anti-tumor effects of temozolomide in vivo but also induced heat shock protein 70-mediated lysosomal membrane permeabilization, a process associated with the release of cathepsin B into the cytosol, which in turn is believed to sensitize the cells to the pro-autophagic effects of temozolomide when grafted in vivo [68]. The gene discussed is GAL; the disease is neoplasm.