HRAS and neoplasm: A recent study showed that forced Gal-1 expression resulted in enhanced H-Ras-GTP membrane association, an increased number of Raf-1 recruitment sites, triggered sustained MEK-ERK pathway activation and enhanced cell transformation.24 The Ras-ERK pathway is required for EMT and contributes to the maintenance of an undifferentiated/mesenchymal state in tumor cells.