A new, elongated mutant of garden pea (Pisum sativum L.) is described, and shown to be conferred by a recessive allele of a new gene, sln. At the seedling stage, the mutant resembles the previously described slender type (genotype la cry (s) ), possessing markedly longer basal internodes than the wild-type. Furthermore, as for la cry (s) plants, application of gibberellin (GA)-biosynthesis inhibitors to the dry seeds (before sowing) did not markedly affect internode length in the mutant. However, the inheritance of the new slender phenotype is unusual, since in crosses between sln and Sln plants the mutant phenotype is absent in the F2 generation, reappearing in the F3. Young shoots possessing the new slender phenotype (sln) contained much higher levels of GA1, GA8, GA20 and GA29 than did wild-type shoots. Mature, near-dry seeds from slender plants contained very high levels of GA20, marginally more GA29, and very little (if any) GA29-catabolite, compared with seeds harvested from wild-type (Sln-) plants. It is suggested that sln may impair the catabolism of GA20 in maturing seeds. As a result, GA20 accumulates and on germination may move into the seedling where it is converted to GA1, promoting elongation growth. A model is proposed to explain the inheritance of the sln phenotype and its physiological implications are discussed. The new sln slender mutation has a different mode of action from the established la cry (s) slender gene combination.