Furthermore, recent studies indicate that cross-talk exists among the PR55α-promoted oncogenic pathways, such as1 the Ras/Raf/MEK/ERK signaling that promotes the activation of YAP and c-Myc by increasing their expression2, β-catenin that synergizes with YAP/TAZ during cancer progression, and3 YAP that is required for KRAS-driving pancreatic tumorigenesis and can compensate for the loss of oncogenic KRAS in the KRAS-addicted pancreatic cells to sustain the malignant phenotypes25–27,53–55. This evidence concerns the gene MYC and cancer.