In this model, the upregulated PSEN1 in colon cancer facilitates PD-L1 truncation via potential proteolytic processing, releasing its active C-terminal fragment, and then induces PD-L1 nuclear translocation through impacts on the multiple components in HDAC2-mediated deacetylation, clathrin-dependent endocytosis, vimentin-associated nucleocytoplasmic shuttling and importin family-mediated nuclear import. The gene discussed is VIM; the disease is colonic neoplasm.