SummaryGenes in the D region of the murine major histocompatibility complex, H‐2, confer resistance to radiation‐induced leukaemia virus.H‐2Dgene control appears to ensue at a step subsequent to virus infection, since elimination of virus infected cells does not become apparent until 3‐5 weeks after virus infection. Nonetheless, almost immediately after virus infection, expression of H‐2D‐coded antigens is markedly elevated on the surface of thymocytes from resistant (H‐2Dd) but not susceptible mice (H‐2Dsor H‐2Dq). This increased H‐2D antigen expression triggers a vigorous cell‐mediated immune response which probably plays a key role in resistance to leukaemia via elimination of virus‐infected cells. A hypothesis is put forth to explain the induction of increased sythesis and expression of H‐2D antigens. This hypothesis postulates that the oncogenic segment of RadLV bears a close resemblance to H‐2.4, the private specificity for H‐2Dd, allowing it to integrate at or near theH‐2Ddmurine gene. Subsequent to integration, the rates of transcription and translation are altered with a resulting increase in cell surface antigen expression. Other p