Our prior studies using PANC1 pancreatic cancer cells had demonstrated that neratinib caused ERBB1 and K-RAS to rapidly localize in vesicles within the cell that co-stained for phosphorylated ATG13 and also with cathepsin B. At 60× magnification we discovered that neratinib as a single agent reduced overall K-RAS and N-RAS expression and caused the staining of both RAS proteins to become punctate (Figure 2). This evidence concerns the gene KRAS and familial pancreatic carcinoma.