By contrast, transgenic cardiac expression of active MEK5α, a full-length splice variant of MEK5 with an intact PB1 domain, failed to induce cardiac hypertrophy but showed an increased recovery and cardioprotection after ischemia [99], suggesting that MEK5-dependent ERK5 activation may protect the heart from stress-induced insults (Figure 4). This evidence concerns the gene MAPK7 and cardiac hypertrophy.