Elucidating the roles for receptor phosphorylation in receptor function is a challenging task, and studies to date have revealed a wide range of roles for receptor phosphorylation. Most of the studies have relied on substituting Ala for Ser to prevent phosphorylation; in some cases Asp or Glu substitutions have been used to mimic the negative charge of a phosphate. Because the size of the Asp or Glu side chain does not mimic the phosphate, changes in structure as a result of the size of the phosphate group are not always reproduced by an acidic residue. One of the first functions identified was sensitivity of transcriptional activation in response to hormone. Mutation of Ser 530 in the hinge region of chicken PR increased the concentration of hormone required for 50% maximal transcriptional activation by 5- to 10-fold although hormone binding affinity was unchanged ( 32 ). Phosphorylation of Ser 305 in the hormone binding domain of ERα may play a similar role because phosphorylation inhibits the acetylation of Lys 303 ( 33 ). Substitution of Arg for the acetylation target, Lys 303 , produces a receptor that is hypersensitive to estrogen ( 34 ). Whereas breast cancer cells that express mutant ERα grow equally well in response to either 10 −12 or 10 −9 m estradiol, wild-type ERα expressing cells require 10 −9 m estradiol for optimal growth. Recent in vitro studies support a role for phosphorylation in directly regulating the affinity of ERα for estradiol ( 35 ). Phosphorylation of ERα with either protein kinase A (PKA) or Src increases estradiol binding affinity about 7-fold. PKA phosphorylates both Ser 236 and Ser 305 ; whether both or only one of these sites modulates hormone binding affinity is unknown. Similarly, although Src phosphorylates Tyr 537 , it phosphorylates one or more additional sites in vitro . Thus, additional sites may participate in the modulation of hormone binding of ERα.
The most commonly used AAS in medicine are testosterone and its various esters (but most commonly testosterone undecanoate , testosterone enanthate , testosterone cypionate , and testosterone propionate ),  nandrolone esters (most commonly nandrolone decanoate and nandrolone phenylpropionate ), stanozolol , and metandienone (methandrostenolone).  Others also available and used commonly but to a lesser extent include methyltestosterone , oxandrolone , mesterolone , and oxymetholone , as well as drostanolone propionate , metenolone (methylandrostenolone), and fluoxymesterone .  Dihydrotestosterone (DHT; androstanolone, stanolone) and its esters are also notable, although they are not widely used in medicine.  Boldenone undecylenate and trenbolone acetate are used in veterinary medicine . 
Tren is an extremely androgenic hormone, and as a result well known for promoting androgenic side effects. Hair loss and acne in men who are predisposed are both possible. Body hair growth is also possible. If you are not genetically predisposed no amount of Tren on earth with cause these issues. The androgenic side effects of Tren are truly based on genetic response. When it comes to hair loss, if you are predisposed to male pattern baldness, meaning at some point you’re going to lose your hair regardless of steroid use , Tren is one of the fastest ways to ensure you lose your hair a little sooner.
Virilization is a serious androgenic side effect of Tren. It is very difficult for a woman to use Tren without some level of virilization and makes it a steroid that’s almost never recommended for female use.
Important Note: The 5-alpha reductase enzyme does not metabolize the Trenbolone hormone. This means 5-alpha reductase inhibitors like Finasteride will not affect the androgenicity of the hormone.