In that regard, considering the peptidase nature of KLK7, it has been stated that insulin is one of its targets [98], findings that drive us to hypothesize that during obesity, KLK7 increases as part of the adipose tissue dysfunction related to obesity, which in turn decreases the insulin circulatory availability, decreasing the ability of this hormone to induce its expected metabolic functions in their target organs. The gene discussed is INS; the disease is obesity disorder.