Recent findings show that Peptidylprolyl Cis/Trans Isomerase, NIMA-Interacting 1 (PIN1) overexpression and subsequent upregulation of RAB2A transcription in breast cancer stem-like cells results in abrogation of ERK1/2 dephosphorylation and inactivation by Dual Specificity Phosphatase 6 (DUSP6), which promotes tumorigenesis [14]. This evidence concerns the gene PIN1 and breast carcinoma.