Bacterial endotoxin was used as a granulopoietic stressor in the RLV-A infected mouse as a means of studying the marrow and spleen CFU-C response to this agent. A control group of phenylhydrazine (PHZ)-treated mice was also employed to induce a reduction in hematocrit levels equivalent to that observed in the early and mid-stage of the disease course and was used to determine whether the cloning observed was a manifestation of RLV-A disease or could be attributed solely to the resulting anemia. Both RLV-A infected and PHZ marrow from mice maintained at a hematocrit of 40% exhibited similar but higher than normal clonogenic capacities, whereas RLV-A (hematocrit 40%) spleen had an expanded number of CFU-C's when compared to PHZ treated (hematocrit 40%) mice. Examination of spleens of endotoxin-treated RLV-A (hematocrit 30%) infected mice indicated a 6 to 7-fold increase in splenic CFU-C numbers compared to endotoxin-treated normal mice. PHZ plus endotoxin-treated normal animals (hematocrit 30%) had splenic CFU-C values which were approximately half those of RLV-A infected (hematocrit 30%) endotoxin-treated animals. Results of this experiment suggest a fully operable but greater than normal CFU-C storage pool in the RLV-A infected mouse spleen which does not seem to be due entirely to the anemia.