Rifampicin-resistant mutants have been isolated from a Micromonospora sp. In one of these, rifampicin failed to inhibit [3H]UTP incorporation in osmotically shocked cells; consequently, resistance was probably not due to the alteration of rifampicin permeability. Parallel to the rifampicin resistance there was a substantial increase in the novobiocin sensitivity of the mutants. Rifampicin-sensitive revertants exhibited their original novobiocin sensitivity. At the same time there was no increase in their sensitivity towards coumermycin A1, an agent of related structure and activity. The possible mechanism for this pleiotropy is discussed.