Indeed, consistently with the close association of AKTIP with the nuclear rim and with lamin A, the analysis of nuclei with either exogenous expression of progerin, or with the endogenous HGPS mutation, reveals that progerin profoundly impinges on AKTIP distribution, which suggests that AKTIP dysfunction could be a co-element in the progeroid disease. Here, LMNA is linked to Hutchinson-Gilford progeria syndrome.