These results are further supported by a previous study in which intracellular Gal-1 induced migration and invasion of glioblastoma multiforme cells.29 However, given that intrinsic Gal-1 can bind to a number of ECM components, such as laminin and fibronectin,28 it remains possible that in the present study, preferential binding of Gal-1 to ECM components interfered with our ability to detect the basal levels of any secreted forms of intrinsic Gal-1. Here, GAL is linked to glioblastoma.