Understanding the mechanistic link between TDO2 overexpression, Trp metabolism and Kyn production, AHR activation, and LM cell function alterations will not only provide critical evidence supporting a causal link between MED12 mutation and the development of LM, but it may also open new avenues toward the development of strategies preferentially targeting the mut-MED12 LM subtype and, thus, precision medicine in the area of uterine LM. The gene discussed is AHR; the disease is lymphangioma.