Because non-genomic pathways include any mechanism that is not a genomic effect, there are various non-genomic pathways. However, all of these pathways are mediated by some type of steroid hormone receptor found at the plasma membrane.  Ion channels, transporters, G-protein coupled receptors (GPCR), and membrane fluidity have all been shown to be affected by steroid hormones.  Of these, GPCR linked proteins are the most more information on these proteins and pathways, visit the steroid hormone receptor page.
Because the ultimate goal of a steroid cycle is to increase strength and muscle size, the associated spike in estrogen which accompanies steroids such as Testosterone is considered undesirable. In order to disassociate the two effects, two classes of drug are used. Medications such as Nolvadex or Clomid target the estrogen receptors. They make it more difficult for the estrogen to exert it’s influence within the body thus allowing the testosterone to act more freely. The second class is aromatase inhibitors such as Femara. They target the aromatase enzyme itself in order to prevent the production of estrogen in the first place. Sometimes, it’s not always clear which option you should go with or even what the differences are between the two. Lets clear that up a little.
Anabolic steroids do have legitimate medical uses. They were first synthesized in the 1930s to treat underdeveloped testes and resulting testosterone deficiency. In the 1950s, they were used to treat anemia and muscle-wasting disorders and to bulk up patients whose muscles had atrophied from extended bed rest. In the 1960s, anabolic steroids were used to treat some forms of dwarfism. Today anabolic steroids are being studied for their ability to alleviate the extreme body wasting associated with acquired immunodeficiency syndrome (AIDS). Their most common use, however, remains among athletes seeking a quick competitive edge.