Stanley Joel Korsmeyer (June 8, 1950 – March 31, 2005) was an American research scientist known for his work on B cell lymphomas and apoptosis.

Born and educated in the US state of Illinois, Korsmeyer spent most of his career as a professor at Washington University School of Medicine and later the Dana–Farber Cancer Institute.

Korsmeyer went on to start his own laboratory at Washington University in St. Louis, further studying the role of Bcl-2 in cell biology.

His group's work expanded the paradigm of cancer-causing genes, providing the first example of how interfering with programmed cell death could lead to cancer development.

[3][4] At some point an early mentor, local veterinarian Robert Goodin, advised him instead to consider a career in biology.

[7][8] Collaborating with Philip Leder's group, Korsmeyer defined the chromosomal translocation that underlay most follicular lymphoma, naming the affected gene Bcl-2.

[5] In 1990, Korsmeyer's group found that Bcl-2 typically resides in mitochondria, sparking further research into how mitochondrial proteins regulate cell death.

They went on to define the mechanism by which mitochondria influence apoptosis – via Bcl-2 and a family of related proteins including BID, BAD, and BAX.

[4] In 1998, Korsmeyer was recruited to Harvard Medical School to serve as the Sydney Farber Professor of Pathology and Medicine as well as Director of the Dana–Farber Cancer Institute's Program in Molecular Oncology.

Without Bcl-2 suppression, BID and other pro-death regulators oligomerize BAX and BAK, initiating the cell death pathway.