Model of ER action at AP-1 sites. The underlying mechanisms of estrogen and anti-estrogen pathways are distinct. In the AF-dependent/Estrogen Pathway: the balance of co-activator and co-repressor functions is altered by the introduction of the K206A mutation. Loss of ER: repressor interactions lead to unopposed, potent, co-activator stimulation (right). In the AF-independent or anti-estrogen pathway, ERs titrate, or functionally inactivate, a repressive function associated with the promoter (left). The K206A mutation renders the ER unable to do so. The star represents a mutation at ERα K206: K > A/G in the AF-dependent pathway; or K > any mutation except arg, in the AF-independent pathway.