To ATCC Valued Customers,

ATCC stands ready to support our customers’ needs during the coronavirus pandemic. If you experience any issues with your products or services, please contact ATCC Customer Service at For Technical questions please contact Thank you.

Privacy Policy Update

We remain dedicated to protecting your data and experience throughout our platforms. We have updated our Privacy Policy and your continued use of the Site means you have accepted the revised Privacy Policy. View now >

Genetic Diseases

Genetic diseases are caused by mutations, duplications, deletions or translocations of genetic material within gametic cells. Mutations that do not produce lethality give rise to individuals that display phenotypic characteristics associated with each disease or syndrome. ATCC provides a wide array of cell lines from genetic diseases, such as Down's Syndrome, Cystic Fibrosis, Cri du Chat Syndrome, and Marfan's Syndrome.
CRL-4013 PDL_01-02_CFTR.jpg

Cystic Fibrosis Cell Lines

ATCC has cell lines derived from cystic fibrosis lung tissue and from iPSCs reprogrammed by episomal expression of the OCT4, SOX2, KLF4, and MYC genes.
55-X-59179020-DAY 14-001.jpg

Down Syndrome Cell Lines

ATCC has cell lines derived from the tissue and iPSC of individuals affected by Down syndrome.
CRL-11386-58483237-DAY 8-001.jpg

Ehlers-Danlos’ Syndrome Cell Lines

ATCC offers cell lines derived from the skin of individuals affected by multiple types of Ehlers-Danlos syndrome.

Hereditary Spherocytosis Cell Lines

The ATCC collection includes several derivations of the WIL-2 cell line, which originates from the spleen of a hereditary spherocytosis patient.
55-X-59179020-DAY 14-001.jpg

Lesch-Nyhan’s Syndrome Cell Lines

The ATCC collection includes cell lines of mouse and human origin to support the study of Lesch-Nyhan’s syndrome.
CRL-11730-58690706-DAY 1001.jpg

Marfan’s Syndrome Cell Lines

ATCC’s holding include an array of cell lines derived from the skin of individuals affected with varying severity by Marfan’s syndrome.