Under the selection exerted by treatment with androgen receptor targeted androgen deprivation therapy, rare subpopulations of cells present in origin tumor foci that reactivate androgen receptors through a variety of molecular processes from the acquisition of mutations; copy number alterations to synthesis of constitutively active androgen receptor splice variants acquire the capacity to evade androgen deprivation therapy, while other cells acquire alterations in MYC and CTNNB1 and develop the capacity to seed and reseed multiple sites through a metastatic process [47,48,49,50]. The gene discussed is AR; the disease is neoplasm.