To investigate the hypothesis that NEPC tumor cells are also capable of activating the MBL complement pathway through the glycosylated cell membrane and to understand the difference in the intrinsic attributes between NEPC and prostate adenocarcinoma (PrAD), which may lead to distinct organotropic metastasis of these two PCa subtypes, we first analyzed the Beltran and SU2C PCa transcriptome datasets.[18] Compared with their PrAD counterparts, the human NEPC biospecimens in both datasets presented a significant hallmark of “cell surface glycosylation” (Figure 2e,f). The gene discussed is MBL2; the disease is posterior cortical atrophy.