Bile acids, in particular chenodeoxycholic acid (CDCA) and cholic acid (CA), can regulate the expression of genes involved in their synthesis, thereby, creating a feed-back loop. The elucidation of this regulatory pathway came about as a consequence of the isolation of a class of receptors called the farnesoid X receptors, FXRs . The FXRs belong to the superfamily of nuclear receptors that includes the steroid/thyroid hormone receptor family as well as the liver X receptors (LXRs) , retinoid X receptors (RXRs), and the peroxisome proliferator-activated receptors (PPARs) .
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.
Most often, raised levels of follicle stimulating hormone are a sign of malfunction in the ovary or testis . If the gonads fail to create enough oestrogen, testosterone and/or inhibin, the correct feedback control of follicle stimulating hormone production from the pituitary gland is lost and the levels of both follicle stimulating hormone and luteinising hormone will rise. This condition is called hyper gonadotrophic- hypo gonadism, and is associated with primary ovarian failure or testicular failure. This is seen in conditions such as Kallmann’s syndrome in men and Turner syndrome in women.