Fanconi anaemia (FA) is an autosomal recessive disorder characterized by a diversity of clinical symptoms including skeletal abnormalities, progressive bone marrow failure and a marked predisposition to cancer^1–4. FA cells exhibit chromosomal instability and hyper-responsiveness to the clastogenic⁵ and cytotoxic⁶ effects of bifunctional alkylating (cross-linking) agents, such as diepoxybutane (DEB) and mitomycin C (MMC). Five complementation groups (A–E) have been distinguished on the basis of somatic cell hybridization experiments^7–9, with group FA-A accounting for over 65% of the cases analysed^10,11. A cDNA for the group C gene (FAC) was reported¹² and localized to chromosome 9q22.3 (ref. 8). Genetic map positions were recently reported for two more FA genes, FAA (16q24.3)¹³ and FAD (3p22–26)¹⁴. Here we report the isolation of a cDNA representing the FAA gene, following an expression cloning method similar to the one used to clone the FAC gene¹². The 5.5-kb cDNA has an open reading frame of 4,368 nucleotides. In contrast to the 63-kD cytosolic protein encoded by the FAC gene, the predicted FAA protein (M_r 162,752) contains two overlapping bipartite nuclear localization signals and a partial leucine zipper consensus, which are suggestive of a nuclear localization.