Mdivi‐1 (mitochondrial fission inhibitor‐1) was originally identified as a selective inhibitor of Drp1, blocking the entire fission machinery (Cassidy‐Stone et al, 2008). When applied in multiple models of neurodegeneration, including ALS, Mdivi‐1 reduced mitochondrial fragmentation and consequently improved cellular health (Cassidy‐Stone et al, 2008; Luo et al, 2013; Bernard‐Marissal et al, 2015). However, the selectivity of Mdivi‐1 for Drp1 a has recently been challenged (Bordt et al, 2017; Smith & Gallo, 2017). Furthermore, because in addition to cell survival, physiological mitochondrial fission plays important roles in cell proliferation and differentiation and maintaining mitochondrial quality, inhibition of physiological mitochondrial dynamics is detrimental. Hence, the use of a specific inhibitor of excessive/pathological mitochondrial fission only, such as P110, as a treatment for these diseases is advantageous.