Although we demonstrate the exclusion of mitochondrial GCN5L1 in HFD‐fed mouse model, further investigation on GCN5L1 translocation and the underlying mechanism in human patients with type 2 diabetes and MASLD is needed to unveil the function of mitochondrial GCN5L1 in insulin sensitivity. The gene discussed is BLOC1S1; the disease is metabolic dysfunction-associated steatotic liver disease.