In addition, some studies have reported the role of LCK in diabetes, indicating that the interaction of protein tyrosine phosphatase with Src kinase Lck is associated with type I diabetes [67,68], and the inhibition of Lck can inhibit T-cell activation to treat type I diabetes [69], whereas ceAF has already been shown to ameliorate inflammatory responses in STZ-induced diabetic mice and to promote healing of diabetic wounds in mice [11]. This evidence concerns the gene LCK and type 1 diabetes mellitus.