Masteron will significantly suppress natural testosterone production making exogenous testosterone therapy important when using this steroid. Failure to include exogenous testosterone will lead most men to a low testosterone condition, which not only comes with numerous possible symptoms but is also extremely unhealthy.
As most will use Masteron in a cutting cycle, it’s very common not to want to use a lot of testosterone due to the high levels of estrogenic activity it can provide. If this is the case, you will find a low dose of 100-200mg per week of testosterone to be enough to combat suppression and give you the needed testosterone.
Once Masteron is discontinued and all exogenous steroidal hormones have cleared your system, natural testosterone production will begin again. Prior levels will not return to normal over night, this will take several months. Due to the slow recovery, Post Cycle Therapy (PCT) plans are often recommended. This will speed up the recovery greatly; however, it won’t bring your levels back to their peak, this will still take time. A PCT plan will ensure you have enough testosterone for proper bodily function while your levels continue to naturally rise and significantly cut down on the total recovery time. This natural recovery does assume no prior low testosterone condition existed. It also assumes no damage was done to the Hypothalamic-Pituitary-Testicular-Axis (HPTA) through improper supplementation practices.
Intravenously administered glucocorticoids , such as prednisone , are the standard of care in acute GvHD  and chronic GVHD.  The use of these glucocorticoids is designed to suppress the T-cell-mediated immune onslaught on the host tissues; however, in high doses, this immune-suppression raises the risk of infections and cancer relapse. Therefore, it is desirable to taper off the post-transplant high-level steroid doses to lower levels, at which point the appearance of mild GVHD may be welcome, especially in HLA mis-matched patients, as it is typically associated with a graft-versus-tumor effect. [ citation needed ] . Cyclosporine and tacrolimus are inhibitors of calcineurin. Both substances are structurally different but have the same mechanism of action. Cyclosporin binds to the cytosolic protein Peptidyl-prolyl cis-trans isomerase A (known as cyclophilin), while tacrolimus binds to the cytosolic protein Peptidyl-prolyl cis-trans isomerase FKBP12. These complexes inhibit calcineurin, block dephosphorylation of the transcription factor NFAT of activated T-cells and its translocation into the nucleus.  Standard prophylaxis involves the use of cyclosporine for six months with methotrexate. Cyclosporin levels should be maintained above 200 ng/ml.  Other substances that have been studied for GvHD prophylaxis include, for example: sirolimus, pentostatin and alemtuzamab.