RET-dependent tumor-intrinsic chemotaxis toward GDNF drives directional migration, whereas nerve-driven neuritogenesis (axon outgrowth toward tumor) supplies contact guidance; co-culture microchannels quantify chemotaxis by cancer-cell flux to nerve-conditioned gradients, and ex vivo nerve-slice or microfluidic axon-outgrowth assays attribute path length and speed to neuritogenesis (22–24). The gene discussed is GDNF; the disease is neoplasm.