One of the most reproducible findings suggest that unrelated genetic deletion distinct from Rpl3l loss-of-function, such as conditional knockout of a cytosolic gene, glutamyl-prolyl-tRNA synthetase (Erps1), or a nuclear-encoded mitochondrial gene family with sequence similarity 210 member A (Fam210a) in CMs, caused heart failure and exhibited simultaneous increase in RPL3 and decrease in RPL3L mRNA and protein expression levels [31,39]. The gene discussed is MIMS1; the disease is heart failure.