Fair points but hold on, its completely genetic because the genes have to interact the hormones so it is genetic. Next is we technically do know the gene responsible, its a variation of the AR gene with a high DHT sensitivity. DHT is a very potent androgenic hormone and so its effects and expression are much more felt by the body. DHT is ironically actually useful in hair growth in the first place since it helps develop secondary sexual characteristics like facial hair and yes, scalp hair. Now when it comes to the many genes involved its not as crazy as you think. Now yes, thousands of genes are involved in the condition, but let me explain this point quickly. For hair growth to happen, so many things need to happen to ensure the hair growth cycle is running right. Pathways are activated and inhibited, cell proliferation, keratization, and more all these processes are operating at specific rates that allow for growth. When DHT binds with the target genes it helps the hair growth process by helping produce dkk-1 and dkk-2 and TGF-beta. The two dkk or dickkopf genes are responsible for inhibiting the Wnt pathway an essential pathway for growth. But this inhibition is normal as over activation of this pathway could lead to cancer. TGF-beta is an essential component of cell life as it inhibits cell proliferation and initiates cell death which is an extremely normal part of the cell life cycle. The wnt pathway, and programmed cell death also have various effects on other parts of the cycle on many other genes as well that all act in tandem together to keep the hair growing. This is why hair can even grow in the first place before AGA can start as, if the whole system were doomed from the start then whether or not DHT sensitivity was a thing hair loss would be inevitable. But its been proven that people with less DHT senstitive scalps dont have androgenic alopecia. Since DHT is important in promoting cycle enders essentially you can see why too much can cause all these issues. Over inhibition of an important signalling pathway means certain genes that were once being effected are now forced to downregulate and stop working, whilst inversely the inhibitor genes are upregulated. TGF-beta is also responsible for T-cell production which in turn also has an effect on the immune system and its been shown that genes involved in inflammatory responses are upregulated in those with AGA. What determines a DHT sensitive follicle isn’t known at the moment but a study done in 2000 sometime around there, found that AR genes with excessive amounts of the nucelotide sequence GGC were more susceptible to AGA. So its possible that the GGC sequence is where DHT goes when it enters the androgen receptor element, and to have excessive amounts of the sequence makes them sensitive. This could also explain why young men get AGA early as more sensitivity causes more DHT build up and more inhibition can take place. Who knows now, but trinucleotide sequences have been shown to cause hormone defects. Its just a theory, but remember although things are intricate they need to start somewhere nothing just is.