ELAC2 and prostate cancer: The differences between the prostate proteomes of the KO and A537T mice revealed that the A537T variant caused greater representation of pathways and processes involved in tumorigenesis and inflammation (Appendix Fig S7A and B), which was even more apparent by 30 weeks in the A537T mice (Appendix Fig S7B), including ERK and Forkhead box class O (FOXO) activation, known to drive prostate cancer epithelial‐mesenchymal transition (Liu et al, 2015b; Shin et al, 2019; Yan & Huang, 2019), supporting our findings that Elac2 mutations can predispose to the activation of tumorigenesis pathways.