I've just read through this study, and for a layman, I'm impressed with the lucidity, logic and efficiency of this study.
My understanding is this first thing about this study is it's not just another "wnt pathway induces hair growth" study. Everybody and their mother at this point knows that disruption of the wnt pathway in dermal papilla cells (DPC)results in imparied hair growth, but they've identified a protein (CXXC5) that interacts with one of the specific elements (Dvl) of the wnt pathway to disrupt it. So they know precisely what is disrupting it and where precisely it is being disrupted.
Then they've shown that CXXC5 is expressed highly in DP cells taken from human scalps with Androgenetic Alopecia. Then they've show that by disrupting CXXC5's ability to interact with Dvl by using a peptide (PTD-BDM) that "get's there before it", kind of how Finasteride does with 5ar, that wnt signaling resumes and the cell resumes its normal functioning, so normal hair growth.
Then they've shown that combining PTD-BDM and a wnt pathway activator (like VPA) makes the effect even more powerful. This is good stuff.
Then they've shown that combining PTD-BDM and a wnt pathway activator and wounding can induce follicle neogenesis.
They're actually dropping new science here. To my understanding what were looking at could be Androgenetic Alopecia's achilles heel.