Genetic ablation of either Erf or Tbl1x (a component of the NCoR1/2 complex) abrogated the Erf-NCoR1/2 interaction and resulted in a severe TSC differentiation defect due to the faulty SE decommissioning, lack of silencing, and persistent expression of the self-renewal marks associated with these SEs (Lackner et al., 2023). Here, ERF is linked to tuberous sclerosis.