Many questions remain regarding the cellular and molecular mechanisms underlying FD phenotypes, particularly since Elp1 has been proposed to mediate several cytoplasmic (e.g. protein trafficking, α-tubulin acetylation, stress signaling, exocytosis, and tRNA modification and translation of codon-biased transcripts) and nuclear (i.e. transcription) functions (Dalwadi and Yip, 2018; Dietrich and Dragatsis, 2016; Lefcort et al., 2017). Here, ELP1 is linked to Fabry disease.