Indeed, similar observations of LAM features in WT cells have been noted in a neural crest cell model.[14] These data suggest perhaps, while loss of TSC2 is critical for disease pathogenesis, the hallmark features of the putative “LAM cell” may already exist in a physiological, if not transient, context (e.g., during development, injury repair, and inflammation). Here, TSC1 is linked to lymphangioleiomyomatosis.