CAMK2G and diabetes mellitus: In the sections that follow, we highlight representative axes: CaMKIIγ–driven nuclear signaling in cancer and therapy resistance; developmental and cardiac mis-specification driven by δ-isoform partitioning (δB/δC/δ9); and epigenetic “memory” wherein class IIa HDAC export and histone marking—and, in diabetes, O-GlcNAc–dependent CaMKII autonomy—stabilize maladaptive transcriptional states [5,6,7,8,9,19,27,33,35,36,60,65].