Pathologically, mutations in SPOP associated with PCa disrupt PDK1 degradation, while mutations within or near the PDK1 degron—either by blocking SPOP binding or inhibiting CK1/GSK3β-mediated PDK1 phosphorylation—enable PDK1 to evade SPOP-mediated degradation 67. This evidence concerns the gene PDK1 and posterior cortical atrophy.