In rats, an intrarenal injection of nickel subsulfide (Ni3S2) regularly caused, within 2 months, an erythrocytosis and eventually a renal carcinoma in 40 per cent of the animals. Despite their great pleomorphism, the neoplastic renal cells appeared to be of the same lineage but showed a pronounced tendency to evolve toward an anaplastic, spindle-cell variant. By electron microscopy, they exhibited varying degrees of differentiation with surface specialization, suggesting an epithelial origin. There was no indication that the erythrogenic and carcinogenic responses to Ni3S2 were interrelated as the high hemoglobin and erythrocyte values tended to retrocede with the development of the renal carcinoma. Other nickel salts and a variety of divalent metallic preparations failed to produce similar changes when administered under identical conditions. The possible mechanism of NI3S2 at the cellular level is briefly discussed.