TSC1 and lymphangioleiomyomatosis: 2) Limited quantity of DNA samples in some patients restrained us to implement further genetic testing; 3) Although some identified novel variants of TSC1/2 were considered to be the likely causes of S-LAM in these patients, further investigations about these variants are required to determine their abnormal functions and pathogenicity underlying the formation of LAM; and 4) the non-TSC1/2 somatic mutations identified in the LAM patients need to be further investigated about their association to the tumorigenesis of LAM.