The high fraction of ACTA2+ and low fraction of PMEL+ cells in culture is consistent with the relative abundance of these markers in heterogenous human LAM lesions.[3] Notably, the percentage of PMEL+ and ACTA2+ cells did not vary between WT and TSC2−/− (Figure S1B,C, Supporting Information). The gene discussed is ACTA2; the disease is lymphangioleiomyomatosis.