Our findings, showing impairments in mitochondrial oxidative phosphorylation after mt-tRF-LeuTAA silencing in insulin-secreting cells, suggest that further investigations are warranted to determine whether a potential link exists between the depletion of mt-tRNA-LeuTAA-derived fragments observed in patients with the A3243G mutation, β-cell dysfunction, and T2D development. The gene discussed is INS; the disease is type 2 diabetes mellitus.