All these observations put together compel us to propose that: (i) cell-autonomous excess un-repaired DNA damage-associated progeroid status is a significant constituent component of DS, (ii) trisomy of DYRK1A causes this (not excluding contributions from other genes in specific cell types), (iii) this can drive a reduction of Lamin B1 levels in a variety of cell types during development, (iv) the above pathogenetic processes can be reversed by an exogenous intervention correcting the excess kinase activity of DYRK1A. The gene discussed is DYRK1A; the disease is Dravet syndrome.