The activation of the cHa-ras oncogene in the EJ/T24 bladder carcinoma cell line was compared with the activation of the same gene in the rat-derived Harvey murine sarcoma virus. The results indicate that, like the human oncogene, the Harvey murine sarcoma virus-borne ras gene owes its oncogenic capacity to point mutations in coding sequences rather than to the alteration in transcriptional control that occurred when the formerly cellular ras sequences were acquired by the virus. The viral gene retained its transforming ability when its transcription was removed from the influence of the retroviral long terminal repeat promoter and was placed under the regulation of the cHa-ras promoter. Conversely, the viral long terminal repeat was insufficient to activate the normal cHa-ras allele when a single copy of such a construct was delivered to a cell by viral infection. In addition to their mode of activation, the biological properties of the EJ/T24 and Harvey murine sarcoma virus oncogenes were compared by infecting newborn mice with chimeric retroviruses bearing each form. The two alleles acted equivalently, causing erythroleukemias and sarcomas with similar kinetics.