In the same year, Takagi et al. [168] demonstrated that HSPB5 phosphorylation and translocation from the cytosol to the cytoskeletal fraction was increased in cultured cardiomyocytes exposed to H2O2 and in murine hearts subjected to ischemia/reperfusion, mediating the cell protective effect exerted in both systems by protein kinase C-related kinase 1 (PRK1 or PKN) activation. The gene discussed is PKN1; the disease is ischemia.