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The gene closest to this hotspot is FOLH1 (folate hydrolase 1) and could thus be the genetic factor that affects this relationship.
The genes that were more highly expressed in carcinomas treated with androgen ablation agents included those encoding AR and steroid biosynthetic enzymes, as well as a suite of genes that have been previously shown to be targets of AR or have been implicated as being regulated by it, including the gene encoding PSA (kallikrein-related peptidase 3), KLK3, and KLK2, as well as DBI, FASN, IL6, SERPINB5, TGFBR3, TMPRSS2, TUBA1, HOXC6, TRG ,and FOLH1. (61-66) Other upregulated genes may represent secondary, indirect effects of androgen ablation that occur later than reactivation of AR.