Pin1 is highly expressed in a majority of cancers [92,93], and elevation in Pin1 levels by either OSM or IL-6 involves the activation of both STAT3 and NF-κB through direct binding with the pSer/Thr-Pro motifs of STAT3 and p65 in the nucleus that results in promotion of STAT3 transcriptional activation [94,95]. This evidence concerns the gene STAT3 and cancer.