Work using kidney-targeted FLCN gene inactivation in mice has indicated that the Raf-MEK-Erk pathway, which is activated in many cancers and regulates cell proliferation (Roberts and Der, 2007), was activated in FLCN-knockout kidneys (Baba et al., 2008). This suggests that an upstream effector of this pathway may be activated by loss of FLCN tumour suppressor function, resulting in cell growth and proliferation within the FLCN-null kidney cell.
