Such molecular mechanisms were studied recently in vivo and revealed that the upregulation of HGK (a component of Mitogen-Activated Protein Kinase Kinase Kinase Kinase 4), Culin 4B (a scaffold protein with oncogenic activity), overexpression of Human Homebox B9 (a key transcription factor that promotes metastases) and low levels of Receptor tyrosine kinase-like receptor (a noncanonical Wnt receptor) play a major role in the aggressive behavior of PCa [27,28,29,30]. This evidence concerns the gene RYK and posterior cortical atrophy.