We used a mouse model where the lamin A/C gene is modified resulting in a loss of the A‐type lamins at the nuclear periphery and integration with the nuclear envelope.[46] Lamin A/C maintains the mechanical tension of the nuclear envelope and has been shown to interact with p16 and p53.[47] We established primary cultures of CFs from lamin A/C null mice between the ages of 4–9 weeks as mice with the mutation are severely runted and die of cardiac failure around 9 weeks. Here, TP53 is linked to heart failure.