One possible explanation of cytoplasmic accumulation of Ep-ICD observed in PCa in our study is provided by a recent study which demonstrated the association between EpCAM and the proteolytic enzyme ERAP2, and described that EpCAM gets cleaved by ERAP2 in the cytoplasm which might explain the increased expression of Ep-ICD in the cytoplasm observed in our study [46]. The gene discussed is EPCAM; the disease is posterior cortical atrophy.