A variety of mechanisms by which BPA may be a triggering compound to autoimmunity have been described, including its impact on hyperprolactinemia, estrogenic immune signaling, cytokine expression, and activation of macrophages, cytochrome P450 enzyme disruption, molecular mimicry to triiodothyronine, and immunoglobulin pathophysiology with increased production of IgA and IgG2a [79]. Here, CD79A is linked to hyperprolactinemia.