Enzymatic and immunoassaies of serum ceruloplasmin were undertaken on serum samples from 100 newborn infants, their mothers, and 100 unrelated women who served as controls. The results indicate that the remarkably low levels of ceruloplasmin oxidase activity observed in the serum of neonates are not due to deficient ceruloplasmin protein synthesis but to defective copper incorporation in the synthesized protein, resulting in excess apoceruloplasmin concentration. Furthermore, serum coppcr studies involving both total and free copper corroborated this conclusion.