Specifically, MOTS-c promoted the differentiation of CD4+CD25+FOXP3+ regulatory T cells (Tregs), which exhibited low glycolytic activity and showed therapeutic potential in type 1 diabetes (T1D) and other autoimmune diseases, through direct inhibition of mTOR complex 1 (mTORC1) signaling in T cells [86]. The gene discussed is CD4; the disease is type 1 diabetes mellitus.