Our data suggests that elevated Gal-3 in pancreatic tumor cells with mutant K-Ras further increases Ras activity by binding Ras to the plasma membrane, where mediates its downstream effectors including Raf/MEK/ERK,PI3K/AKT and RalA (Figure 6B), thereby inducing pancreatic cancer cell growth and invasion in vitro and in vivo. The gene discussed is KRAS; the disease is familial pancreatic carcinoma.