This editorial refers to ‘The promoter activity of human Mfn2 depends on Sp1 in vascular smooth muscle cells’ by E. Sorianello et al. , pp. 38–47, this issue. Sorianello et al. 1 provide important new information on the regulation on mitofusin (Mfn)2 expression. Mitochondrial fission and fusion were first described in yeast in the 1990s and found to be processes that are essential to maintain healthy mitochondria. Key findings from this work include that mitochondria continuously divide and fuse (fission and fusion), that fission and fusion are essential to maintain mitochondrial health (although the exact reason for this is a subject of debate), and that mitochondria exist as interconnected networks.2 Fission and fusion occur as frequently as every 2min in yeast, but are thought to occur much more slowly in mammalian cells, taking hours or longer.3,4 There initially had been scepticism that the mitochondria in the highly organized and densely packed cardiac myocyte would be able to undergo fission and fusion, but it is becoming clear that fission and fusion are important processes in all cells.5,6 It is increasingly evident that abnormal fission and fusion contribute to cardiovascular disease.7 OPA1 has been found to be decreased in ischaemic cardiomyopathy, while Mfn1/2 were increased …