While reduced proliferation may seem paradoxical given the proven role of FLCN as a tumor suppressor, this observation is in line with our previous studies of FLCNKO RPTECs, which experience a growth disadvantage upon folliculin loss due to induction of a non-canonical interferon response, counterbalancing the TFE3/TFEB-directed hyperproliferation upon folliculin loss (11). The gene discussed is FLCN; the disease is neoplasm.