SummaryMouse strains differ widely in their natural killer(NK)‐cell activity. In the (A X B6) X A backcross, high reactivity was linked to H‐2b, although non‐H‐2‐linked genes were also demonstrated (Petranyi et al., 1975). Harmon et al. (1977) demonstrated an H‐2Dd‐associated reactivity gene (1977). In the present study, we have tested eleven B10 congenic strains for NK activity. The H‐2Dd strains B10.A, B10.T(6R), B10.S(7R), B10.HTT and B10.D2 were more highly reactive than B10, B10.S, B10.G, B10.A(2R) and B10.BR, which do not carry the d allele at the H‐2D locus. While this confirms the H‐2Dd association of a reactivity gene, an exception was found in the B10.A(5R) strain that was low reactive in spite of the fact that it carries H‐2Dd. This suggests the possibility that the H‐2Dd‐associated gene is outside H‐2, to the right of Tla.The AKR.H‐2b congenic line had the same low activity as the AKR.H‐2k strain; both were much lower than B6. This suggests either one of two possibilities: the H‐2b‐linked reactivity gene is relatively distant from the H‐2 complex, although localized on chromosome 17 or alternatively, if localized within or in the close neighbourhood of H‐2, it requires non‐H‐2 genes for full expression.Previously, we have shown that the B6 X DBA/2 F1 hybrid was more highly reactive than either one of its two parental strains (Klein et al., 1978). A similar complementation effect is described in the present paper for the B10.D2 congenic strain. The high reactivity of this line can be due to the combined effect of an H‐2b‐linked gene from DBA/2 and the non‐H‐2 background of B10 or, alternatively, the former, together with an H‐2b‐linked gene from B6 that lies well outside outside the H‐2 locus itself.