Increased serum insulin/IGF-1 significantly correlates with a higher dietary glycaemic load, which is a common finding in acne patients, activates mTORC1, causing IR via ribosomal protein S6 kinase b1 (S6K1), and inhibits FoxO1 which represses androgen signaling, resulting in sebaceous gland dysfunction [47,48]. This evidence concerns the gene INS and acne.