A Hair-Growth Brake Gene, and What Happens When It's Actually Gone

A study set to appear in the August 2026 issue of the Journal of Investigative Dermatology reports that FLCN, the gene mutated in Birt-Hogg-Dube syndrome, acts as a brake on human hair growth. Working with hair follicles removed during transplant surgery and kept alive in organ culture, researchers at Newcastle University and the University of Miami, among them William Fostier and Ralf Paus, found that silencing FLCN kept the follicles growing longer, apparently by sustaining activity in a cell-growth pathway called mTORC1 inside the follicle.

The result extends a line of work the same lab opened in 2023, when it showed, in the identical organ-culture system, that rapamycin, a drug that blocks mTORC1, prolongs the growth phase of cultured human follicles and raises pigment production by increasing follicle levels of a hormone called alpha-MSH. That earlier paper proposed testing mTORC1-blocking drugs for hair loss and graying. Read on its own, the new FLCN paper looks like a sequel: another lever on the same brake, another candidate target for a future treatment.

The gene already has a natural experiment

FLCN was not chosen at random. It is the single gene known to cause Birt-Hogg-Dube syndrome, an inherited condition in which a person carries one working copy instead of two. The syndrome usually appears in a person's twenties as multiple fibrofolliculomas, small dome-shaped bumps that grow from hair follicles on the face, neck and upper body, alongside a lifelong risk of kidney tumors and, according to the clinical reference StatPearls, a roughly one-in-four chance of a collapsed lung between the third and sixth decades of life.

What fibrofolliculomas are not, by that same reference, is more hair. Their epithelial strands never differentiate enough to form a hair fiber, and the follicles lack the inner and outer root sheath a working hair bulb needs. The one population that has lived for decades with reduced FLCN function does not grow fuller hair. It grows disorganized, non-hair-producing follicular tissue instead.

That gap is worth sitting with, not resolving. An organ-cultured follicle is silenced for days to weeks, cut off from the immune system, hormones and the years of cell turnover a real scalp experiences. A person with a Birt-Hogg-Dube mutation lives with partial FLCN loss for decades, inside the full body. The two settings are not measuring the same thing, and nothing published yet shows that briefly dialing down FLCN with a drug would behave like either one.

Questions worth carrying forward

• Does silencing a follicle for weeks in a dish predict what years of reduced FLCN activity do to that same follicle, or diverge from it in ways only time reveals?
• If FLCN suppression were ever developed into a topical hair treatment, what would distinguish that process, mechanistically, from the one that builds a fibrofolliculoma?
• Before this becomes a hair-loss headline, what would the clinicians who already treat Birt-Hogg-Dube patients want asked first?

None of this makes the new finding wrong. It makes it early, and it makes the syndrome the gene is named for the more informative reading, for now.

Sources: PubMed · EMBO Reports via PMC · StatPearls via NCBI Bookshelf