As detected in T1DM patients, cardiac dysfunction, hypertrophy, and fibrosis were demonstrated by upregulation of PKCβ [96] or by downregulation of GLUT4 [97–99], phosphoinositide dependent kinase-1 (PDK1) [100], phosphoinositide-3 kinase (PI3K) [101], or glucokinase (GCK) [102] genes (Table 2). Here, GCK is linked to type 1 diabetes mellitus.