The overexpression of KLK2 and KLK4 genes is highly correlated with cancer occurrence, promoting cell invasion and/or cell metastasis [21,22,23,24,25,26]; the suggested mechanism indicates that KLK2 and KLK4 are involved in modulating insulin-like growth factor binding protein-3 (IGFBP-3) degradation in PCa, resulting in cell proliferation and cancer cell survival [11,27,28]. The gene discussed is IGFBP3; the disease is posterior cortical atrophy.