Moreover, ATP5F1B was phosphorylated in vivo, and the levels of a downregulated ATP5F1B phospho-isoform in diabetic muscle correlated inversely with fasting plasma glucose levels.277 A subsequent study on mitochondrial OXPHOS protein phosphorylation reported that abnormal site-specific phosphorylation of ATP5F1B, together with reduced OXPHOS protein content, contributed to mitochondrial dysfunction during muscle insulin resistance.278 Recent studies have even described an accurate mitochondrial protein atlas of T2D pathological states. This evidence concerns the gene ATP5F1B and Insulin resistance.