The most common cause of functional PTEN loss in prostate cancer is genomic homozygous deletion of PTEN. However, several other mechanisms have also been reported, including inactivating somatic mutations (predominantly frameshift or non-sense truncating mutations), suppression of PTEN-targeting microRNAs (miRNAs) and inactivating post-translational modifications (e.g., phosphorylation and ubiquitylation) [7,8,9,10,11]. This evidence concerns the gene PTEN and Familial prostate cancer.