As mentioned above, TSC2-deficiency results in internalization of E-cadherin leading to EMT; moreover, when LAM patient-derived cells are exposed to estrogen, E-cadherin expression is decreased and N-cadherin is upregulated, similar to the segregation of the germ layers during neurulation (Gu et al., 2013). The gene discussed is TSC2; the disease is lymphangioleiomyomatosis.