ENTPD5 and obesity due to melanocortin 4 receptor deficiency: ENTPD5 not only hydrolyzes ATP but also interacts with fibroblast growth factor 23 and sodium‐dependent phosphate transporter 2a, participating in biological processes like bone metabolism.[36] Our study demonstrated that inhibition of hepatic ENTPD5 played important roles in triggering the development and progression of obesity and metabolic disorders.