Gaucher's disease is a somewhat rare familial disturbance of the cellular metabolism in the reticulo-endothelial cells and histiocytes, characterized by an accumulation and retention of the cerebroside kerasin. Thannhauser and his associates (1) explain this deviation from the normal lipid metabolism as an imbalance of intracellular enzymes concerned with the disintegration and synthesis of sphingomyelin and kerasin within the cell and a resulting accumulation of kerasin. The clinical manifestations may be enlargement of the spleen, liver, and sometimes the lymph nodes, pigmentation of the skin, pinguecula-like lesions of the conjunctivae, thrombocytopenia, and frequently a leukopenia. There may be pain in some portion of the osseous system caused by destructive infiltration of the cerebrosidic reticulosis of the bone marrow, and osseous involvement may be the earliest and continue to be the predominating manifestation of the disease. An accompanying fever and leukopenia are usually present. It is of the predominantly osseous type with which this case report deals. Risel (2) was the first to note macroscopic bone changes in Gaucher's disease and described the spongiosa at the upper and lower ends of the femur dotted with rather small, thick, whitish areas, arranged in a stellate form either in nodes or streaks or in a net-like manner. These areas represented deposits of Gaucher cells. The first complete x-ray studies were made by Klercker (3) and Junghagen (4) in 1926. The earliest as well as the most consistent type of change usually occurs as a widening of the lower ends of the femur, just above the condyles (Fischer's sign). This is followed by areas of rarefaction with intermingled areas of sclerosis and a resulting club-shaped conformation. The severe pain over this region when the changes begin to take place, accompanied by fever, makes it easy to confuse this condition with acute osteomyelitis. A history of some preceding trauma can almost always be obtained and, despite the low-grade fever and lack of leukocytosis, operation may be performed. The finding of a sterile pus from which no organism can be grown, coupled with the other findings atypical of acute osteomyelitis, may help to throw doubt on this diagnosis. Once operation has been done, drainage may continue for months. Bony changes occur frequently in the humerus, tibia, fibula, radius, ulna, and ribs. Changes have also been described in the pelvis and skull. Of those cases described in the literature, the most common changes in the long bones include general osteoporosis, large areas of destruction of the spongiosa, and as a late manifestation punched-out areas in the bone with irregular thickening of the cortex. Pathological fractures have been noted in long bones with a destructive lesion. Similar destructive changes in the head of the femur may result in a deformity which must be differentiated from Legg-Perthes' disease, tuberculous coxitis, and chronic osteomyelitis.