Based on this reasoning, more recent studies corroborate the hypothesis that E-cadherin might be a new substrate for matrilysin, which suggests that cleavage of the E-cadherin ectodomain might be required for lung epithelial repair [148] or as a new mechanism to explain the invasive potential of oral squamous cell carcinomas [149] and prostate cancer [150]. This evidence concerns the gene CDH1 and Familial prostate cancer.