The enrichment of neuronal/synaptic modules (e.g., neurexin/neuroligin and L1CAM interactions) plausibly reflects two non-exclusive processes in bladder cancer: (i) reuse of synaptic/adhesion machinery by tumor cells to modulate cell–cell and cell–matrix communication, migration, and plasticity, and (ii) potential nerve–tumor interactions within the bladder microenvironment. The gene discussed is L1CAM; the disease is urinary bladder carcinoma.