Using the tissue culture of the bone marrow, I have studied the mechanisms of adrenalin cortisone and ACTH eosinopenia in the bone marrow. The results are as follows: (1) For the mechanism in the bone marrow, adrenalin eosinopenia is based on checking or migratory impossibility of the eosinophil to the bone marrow sinus, and not on the reduced production of the bone marrow. (2) Cortisone eosinopenia is caused from the hypofunction of the eosinophil or from developmental disturbance of the bone marrow parenchyma. (3) Adrenalin or cortisone eosinopenia greatly depends upon its quantitative proportion in the medium. (4) For the direct effect on the bone marrow, ACTH causes the hyperfunction of the eosinophil in a paticular manner but has no influence upon the cell division of the eosinophil. (5) The pseudoeosinophil is free from hypofunctional action and developmental disturbance of adrenalin, cortisone, or ACTH, except the case of high concentration of adrenalin as well as cortisone.