Our recent publication in Molecular Biology of the Cell was highlighted and given the cover! Chromatin histone modifications and rigidity affect nuclear morphology independent of lamins. This study reveals it’s what’s on the inside that counts to how you look on the outside…for a nucleus. We report that chromatin decompaction via increasing euchromatin or decreasing heterochromatin results in a softer nucleus that can no longer maintain normal shape and thus presents abnormal nuclear blebbing, independent of lamin perturbations. Conversely, increasing heterochromatin stiffens the nucleus and rescues nuclear morphology in lamin-perturbed cells that present abnormal nuclear morphology. Abnormal nuclear morphology is a hallmark of many human diseases including heart disease, muscular dystrophy, aging, and many cancers. We revealed that in model cells and patient cells of advanced aging disease progeria caused by mutant lamin A, which presents depleted heterochromatin levels and abnromal morphology,  nuclear morphology can be rescued by restoring heterochromatin levels.  These findings clarify that lamins are not the sole determinant of nuclear mechanics and morphology, and that chromatin’s role in nuclear mechanics is essential to an entire force response regime (Stephens et al., 2017) and nuclear morphology (Stephens et al., 2018, this paper).