The current understanding is that MA develops through transdifferentiation from predominantly endometrioid Müllerian lesions, which is further supported by a high frequency of associated endometriosis in MA (62% in the current study, which is nearly identical to the rate of 63% reported in a recent study on extrauterine MA [26]) as well as the loss of ARID1A expression observed in a subset of MA in the current study. The gene discussed is ARID1A; the disease is microtia.