Our results showed that only ADAM17 knockdown remarkably reversed both the increased shedding of E-cadherin (Figures 4(a) and 4(b)) and the enhanced cell migration (Figure 4(c)) by CD82 silencing the most among all four ADAMs, implying that the effects of CD82 in E-cadherin shedding in PCa cells might be mediated by ADAM17. The gene discussed is ADAM17; the disease is posterior cortical atrophy.