The results of the cell–cell interaction network analysis disclosed the higher interactions of TRIB3high tumor epithelial cells with other cell types in certain ligand–receptor pairs, spanning CD70-CD27, CLEC2B-KLRB1, CD99-CD99, COL6A2-CD44, COL6A2-SDC4, PGD-VEGFR1, and PROS1-AXL, suggesting that the TRIB3high subset showed stronger local interactions with other major cell types (Supplementary Figure S9), which could predispose to an increased ability of induction and reprogramming of extrinsic phenotypic features, thereby reshaping the overall TME. The gene discussed is AXL; the disease is neoplasm.