In the PT group, Delta Like Canonical Notch Ligand 1 (DLL1)-mediated canonical NOTCH pathways were universally activated via interactions between iCAF and many other cells, which corresponded to its favorable role in anti-cancer immunity in lung cancer [52,53,54], while instead, there were enriched activations of noncanonical NOTCH pathways via interactions of Delta-like Noncanonical Notch Ligand 1 (DLK1)-NOTCH between cancer cells and pericytes (the immature type for NOTCH1, NOTCH2 and NOTCH3; the differentiated type for NOTCH1, NOTCH2, NOTCH3 and NOTCH4) in the BM groups (Figure 6C). This evidence concerns the gene DLK1 and lung cancer.