For example, elevated JNK activity in breast cancer did not induce apoptosis as expected, but cell migration and EMT, along with an enhanced expression of vimentin and AP-1.35 In addition, targeting of RAS/JNK eliminated CSC features and prevented tumor formation in pancreatic cancer.36 Similarly, a pivotal role of JNK in the maintenance of self-renewal and tumorigenicity in glioma stem-like cells was demonstrated.37 Moreover, AP-1 was defined as a critical regulator of a complex program of gene expression mediating an invasive phenotype.27 This evidence concerns the gene VIM and pancreatic neoplasm.