named after Hershey's Kisses
1996 (gene discovery and naming); 2003 (reproductive/puberty role discovered)
A gene named as an inside joke about a small-town chocolate factory turned out, seven years later, to be the master switch that starts human puberty.
In 1996, in a cancer lab at Penn State College of Medicine in Hershey, Pennsylvania — the very town built by the Hershey's chocolate company — Danny Welch's group (with lead author Jong-Hwan Lee) went hunting for a gene that stopped melanoma from spreading. Fusing melanoma cells with chromosome 6 and sifting through the results, they pulled out a novel gene that, switched back on, slashed metastatic spread by more than 95 percent while leaving the original tumor untouched. It needed a name, and the lab had a sense of humor: they called it KISS1 — the 'SS' for 'suppressor sequence,' the 'KI' a nod to the lab's naming habit and, in the words of a later nomenclature review, chosen 'with a bit of whimsy' so everyone would know it came from Hershey, home of the famous Hershey's Kisses.
For years the gene led a quiet life in oncology, nicknamed metastin for its anti-metastatic day job. The twist arrived from a totally separate field: in 1999 researchers cloned a lonely 'orphan' receptor called GPR54 with no known partner, and in 2001 kisspeptin — the same Hershey-named cancer peptide — turned out to be exactly what it had been waiting for. Then, in late 2003, two independent teams (Nicolas de Roux's in France and Stephanie Seminara's collaborators in the US) each reported that families carrying broken versions of that receptor never entered puberty at all — and mice engineered to lack it did the very same thing. A gene christened as a chocolate joke had turned out to sit at the very top of the reproductive cascade: kisspeptin neurons are the gatekeepers that switch on the GnRH neurons driving puberty, ovulation, and fertility in both sexes.
The coincidences didn't stop there. In the hypothalamus, kisspeptin neurons ride alongside two other peptides — dynorphin and neurokinin B — and reproductive scientists now routinely call the trio KNDy, pronounced 'candy.' And the story circled back to romance in 2017, when an Imperial College London team led by Waljit Dhillo and Alexander Comninos infused healthy men with kisspeptin and watched, on fMRI, brain regions tied to sexual arousal and romantic attraction light up while negative mood dimmed — an early hint that this reproductive hormone also shapes desire inside the brain, not just the plumbing downstream.
True. The chocolate origin really is real — the 1996 discovery paper carries a Hershey, Pennsylvania address, and multiple independent naming-history reviews confirm KISS1 was christened as a wink at Hershey's Kisses. The jaw-dropping sequel holds up just as well: two separate teams, publishing independently in 2003, each showed that breaking this gene's receptor stops puberty in its tracks, with a matching mouse phenotype to back it up.
No kisspeptin drug is FDA-approved as of 2026, but research runs on two tracks. In fertility medicine, kisspeptin-54 has been tested as a gentler IVF ovulation trigger for women at high risk of ovarian hyperstimulation, and newer receptor agonists like MVT-602 can reproduce a more natural LH surge than existing trigger drugs. In sexual medicine, the Imperial College brain-imaging work has grown into trials for hypoactive sexual desire disorder and hypogonadism. Still, in October 2024 the FDA's compounding advisory committee voted against approving kisspeptin-10 for compounded use in secondary male hypogonadism — so despite the famous origin story and two-plus decades of study, kisspeptin remains an investigational compound, while KISS1's original cancer-suppressor role stays an active, separate oncology question.
