In line with nuclear positioning and cell polarization defects observed in laminopathies or upon alteration of Lamin A, Emerin, or LINC complex in fibroblasts or myoblasts [51], we also demonstrated that, similarly to TRF2 knockdown, also silencing of Emerin, direct TRF2-interactor, induced polarization defects in our TNBC model and that combined knockdown of TRF2/Emerin didn’t show an additive effect, suggesting that the two proteins are acting on the same axis. Here, EMD is linked to laminopathy.