The linear ubiquitination of phosphatase and tensin homolog (PTEN) leads to a pronounced loss of its activity, a process that enhances phosphoinositide 3-kinase (PI3K)/protein kinase B (AKT) signaling, thereby driving the progression of prostate cancer (PCa) in patients and potentially increasing the risk of recurrence [122]. This evidence concerns the gene AKT1 and posterior cortical atrophy.