On the other hand, the severe hemolytic anemia observed in this model, which is not a common trait in human GSD-VII patients, is explained by the different composition of the PFK-M and PFK-L isoforms in human and dog erythrocytes (i.e., PFK-M accounts for 40–50% of total enzyme expression in humans, vs. 80–90% in dogs). The gene discussed is PFKM; the disease is glycogen storage disease VII.