To investigate if senescence could contribute to the LAM development and progression, we studied the senescent features of a LAM cell line, the human primary LAM/TSC cells isolated from chylous thorax of a patient affected by LAM associated to TSC [16], and of PLFs, obtained from a lung biopsy, which express tuberin and do not display mTOR hyperactivation (Figure 1a). The gene discussed is TSC2; the disease is lymphangioleiomyomatosis.