Conversely, expression of a Spry2 gain-of-function transgene in the context of Pten homozygosity suppressed the AKT hyperactivation, and the prostate tumorigenesis resulted from Pten loss-of-function, implicating the Sprouty genes in regulation of ERK and PI3K/AKT pathways in prostate cancer. This evidence concerns the gene AKT1 and Familial prostate cancer.