The interaction between progerin and Ca2+‐regulating proteins (e.g., Sln and Calnexin) provides a molecular explanation for the multitude of metabolic phenotypes (Figures 2, 3, 4), such as muscle weakness and malfunctioning lipid turnover in laminopathies (Liao et al., 2016; Worman, 2012). This evidence concerns the gene SLN and laminopathy.