The minimal response of p-ERK1/2 and p-AKT in 1,3,4-O-Bu3ManNAc-treated cells can be explained by activation of ERK1/2 and AKT via RAS [35, 55]; mutations that constitutively activate RAS signaling have long been associated with non-small cell lung cancer and metastatic colorectal cancer [56] and now have been linked to pancreatic cancer. The gene discussed is AKT1; the disease is pancreatic neoplasm.