Given that nuclear activity of CaMKIIδC has been shown to lead to prosurvival mechanisms within cardiomyocytes and reduced pathologic remodeling (Little et al., 2009; Peng et al., 2010; Lu et al., 2011b), the manipulation of CaMKIIδ at the splicing level through RNA-based mechanisms offers a theoretically plausible mechanism for improving HF treatment that might not even require targeting CaMKII inhibition. Here, CAMK2G is linked to hydrops fetalis.