Lastly, the novel mechanisms include functional heterogeneity where malignant subclusters in CRC tumors drive progression via HDAC inhibitor-responsive genes (ATF3/CAV1), inflammatory mediators (LXN/PGM1, TMSB4X) and the stromal-tumor crosstalk for tumor progression and immune evasion (C5AR1-RPS19 axis). This evidence concerns the gene LXN and neoplasm.