Hell, I got an idea(a little bit off topic) that although AA & Androgenetic Alopecia have huge difference in mechanism, JAK suppressor like ruxolitinib & tofacitinib can also do some help to male pattern baldness. From what i understand, the pgd2-gpr44 reaction, is actually a "triggering" of th2 cell, like in atopic dermatitis and asthma etc. We can naturally think that if we kick away the th2 **** by any means(the same logic stands in treatments of many other immune diseases including asthma), things should get better. JAK pathway is crucial in most th cells, and I once read that tofacitinib as a JAK3 suppressor may have higher effect on th2. Why the heck such strong immune inhibitors can't do anything on male pattern baldness?PGD2 suppression is still only one aspect of Androgenetic Alopecia. May not do anything for us. Given that DHT is only one of many culprits in Androgenetic Alopecia and balding continues while blocking it completely, it only proves that there's much more to Androgenetic Alopecia than a single pathway. So... PGD2 may exhibit similar problems. Personally, I don't think addressing PGD2 is going to cut it. Probably some reversal and a more guaranteed halt to hair loss, but not a complete solution like arthritis drugs for AA. Something much bigger than PGD2 and DHT imo needs to be addressed... if not, then all pathways simultaneously.