Stanford et al. also reported that TSC2-deficiency represents a barrier to reprogramming (53), while TSC2-happloinsufficient allowed iPSC generation with TSC2+/−-iPSC-derived smooth muscle cells recapitulating Lymphangioleiomyomatosis (LAM) features including increased mTORC1 activation, abnormal autophagy and LAM-associate biomarker expression (53). The gene discussed is TSC2; the disease is lymphangioleiomyomatosis.