This conclusion is supported by the following observations: (1) Infection of Ad-SIRT6 or transfection of WT-SIRT6 plasmid reversed PE-induced upregulation and dephosphorylation of NFATc4, coordinating with the changes of cardiomyocyte surface area and hypertrophic gene BNP expression (Figures 3, 4); (2) SIRT6 overexpression inhibited PE-induced NFATc4 nuclear shuttling (Figure 5); (3) The effect of SIRT6 on repressing BNP expression was reversed by NFATc4 replenishment (Figures 7A–C); (4) SIRT6 deficiency-mediated BNP upregulation was recovered by NFATc4 silencing (Figures 7D–F). The gene discussed is SIRT6; the disease is infection.