Our findings demonstrate that CgA depletion in neuroblastoma cells resulted in a cell morphological shift associated with increased expression of Schwann and ECM specific molecules (PMP22, SERPINF1, FN, LAMB2 and COL4A1), and suppression of features associated with the chromaffin phenotype (reduced IGF-II). The gene discussed is COL4A1; the disease is neuroblastoma.