Testicular teratomas can be experimentally induced in some strains of mice by grafting 12-\or 13-day male genital ridges to the testes of adults. The grafts develop into testes and teratomas can be recognized histologically in them about a week after grafting. Some strains are more susceptible to experimental teratocarcinogenesis than others, and strains 129 and A/He are more susceptible than any others tested. F1 hybrids between these strains are even more susceptible than either parent strain. This suggested that strain A/He may have a gene or genes lacking in strain 129 that influence susceptibility to experimental teratocarcinogenesis. To test this hypothesis we made several recombinant inbred (RI) strains using strains 129 and A/He as progenitors. Each of the RI strains should have half of its genes derived from one progenitor and half from the other, and each RI strain should have a different combination of fixed genes. Nine strains have been inbred for more than twenty generations of brother times sister matings. Four of these new RI strains are more susceptible to experimental teratocarcinogenesis than either parent strain, three are less susceptible, and two are about the same. This indicates that some of the genes that determine susceptibility are the same in both parent strains. It also indicates that strain A/He has a gene or genes lacking in strain 129 that increases susceptibility to experimental teratocarcinogenesis. Reciprocal crosses were made between RI lines and between RI lines and the parental strains. There was no evidence for a maternal influence on the inheritance of susceptibility. Even though some RI strains are highly susceptible to experimental teratocarcinogenesis, they rarely if ever have spontaneous teratomas. A recently identified gene, named teratoma (ter), dramatically increases the incidence of teratomas in strain 129 mice. It also causes teratomas in the susceptible RI strains. (M)