Summary Clinical B12 deficiency is further characterized by accumulation of S. fae-calis-active folyl monoglutamates after 5 mg of oral PGA. B12 treatment lowers S. faecalis activity to normal implying that B12 decreased folyl monoglutamate activity; neither normal nor folate-depleted subjects showed this effect. Our findings suggest that B12 deficiency interferes with formimino transfer-ase, and that principally PGA, not N5-methyl THF, accumulates during B12 deficiency. We thank Mrs. Susan Feingold for her assistance in this study, and Dr. J. M. Ruegsegger, Lederle Laboratories, Pearl River, N. Y., for gifts of folates.