Multiple mechanisms, such as the overexpression of immune checkpoint molecules, loss of nutrients through vascular impairment and dysregulation of metabolic pathways, were recently shown to affect T cell recruitment and metabolic activities in the tumor microenvironment (TME) (56, 57) Preclinical models and human studies of immunotherapy suggested that the general pathology of common forms of diabetes, namely, insulin resistance (T2DM) and/or impaired insulin secretion, may be exacerbated by ICIs (58). This evidence concerns the gene INS and neoplasm.