Genetic deletion or therapeutic inhibition of miR-208a has been previously associated with enhanced cardiac function in a model of pressure overload in mice.53,54 In the context of ischaemic injury, we could show that anti-miR-mediated targeting of miR-208a increases ZEB2 expression and ameliorates cardiac hypertrophy and dysfunction (see Supplementary material online, Figure S6, and Figure 6). The gene discussed is ZEB2; the disease is cardiac hypertrophy.