A recent report from Zhong et al. (2016) describes FLCN as a ciliary protein that regulates mTORC1 through primary cilia. The study shows that in response to flow stress, FLCN recruits the kinase LKB1 to primary cilia for activation of AMPK at the basal bodies, causing mTORC1 down-regulation. The results demonstrate that FLCN, the tumour suppressor associated with BHD, is part of a flow sensory mechanism that regulates mTORC1 through primary cilia. These findings should help to better understand BHD pathogenesis as a ciliopathy.