The authors [66] concluded that MetS may affect male fertility by way of the following mechanisms: (i) at the molecular level, inducing the pro-apoptotic CIDEA, leading to sperm DNA fragmentation and insulin gene expression, and (ii) through a “spermatozoa insulin resistance”, considered to be a part of MetS-related insulin resistance, characterized by increased sperm insulin gene expression, as well as increased seminal insulin and glucose levels. This evidence concerns the gene INS and metabolic syndrome.