Chromosomal alterations and rearrangements, the loss of phosphatase and tensin homolog (PTEN) and activation of phosphoinositide 3-Kinase/-mammalian target of rapamycin (PI3K/mTOR), the increased expression of interleukins and growth factors, global defects in apoptosis, and the loss of function of the prostate tumor-suppressor gene NKX3 are other molecular aberrations associated with PCa [20,21,22,23,24] (Figure 4). The gene discussed is MTOR; the disease is posterior cortical atrophy.