It is known ERK1/2 1) promotes tumor progression, 2) is often hyperactivated due to frequently mutated RAS signaling and 3) promotes mitochondrial fragmentation through phosphorylating residue S616 on DRP1 (Kashatus et al., 2015; Serasinghe et al., 2015; Guo et al., 2020). Here, DNM1L is linked to neoplasm.