On the other hand, we found that while ~1.0% of 245 cases affected by 252 mutations across 27 projects was attributable to aim/cd5l gene mutation in PRAD, these were associated mainly with the loss of gene function copy number variation (CNV) (Figure 2D), thus explaining the very mild or null expression of AIM in Figure 1E. These data indicate that aberrantly expressed PSA and significantly suppressed AIM expression characterize advanced stage prostate cancer, regardless of mutation status. This evidence concerns the gene KLK3 and Familial prostate cancer.