Members of the Snail gene superfamily, which encode zinc finger transcriptional repressors, play critical roles in the establishment of the vertebrate body plan. The Snail1 (Snai1) gene promotes epithelial–mesenchymal transitions during development and disease progression, and Snai1 null mouse embryos exhibit defects in gastrulation. However, the early embryonic lethality of Snai1 null embryos precludes the study of Snai1 function in other developmental contexts or diseases. To overcome this restriction, we generated a Snai1 conditional null allele by flanking the promoter and first two exons of the Snai1 gene with loxP sites. Cre‐mediated deletion of the Snai1^flox allele generates the Snai1^del2 allele, which behaves genetically as a Snai1 null allele. This conditional null allele will enable investigation of Snai1 function in a variety of developmental and pathological contexts. genesis 44:7–11, 2006. © 2006 Wiley‐Liss, Inc.