Also, treatment with either AT1 receptor blocker or tempol attenated STZ-induced cardiac hypertrophy and fibrosis by attenuating the inactivation of GSK3β and thus preventing the nuclear translocation of NFATc3, and also attenuated PKCβ2 and p38 MAPK signaling 28 days after STZ injection. The gene discussed is GSK3B; the disease is cardiac hypertrophy.