Triosephosphate isomerase deficiency
Unlike most of the cells in a human body, erythrocytes (or red blood cells) don't have mitochondria (because they are basically O2 carriers), and don't perform Krebs Cycle or Oxidative Phosphorylation. Therefore, they depend exclusively on glycolysis to produce their ATPs.

According to the Genetics Home Reference (from the NIH, National Institutes of Health) page about triosephosphate isomerase deficiency:


  The anemia in this condition begins in infancy. Since the anemia results from the premature breakdown of red blood cells (hemolysis), it is known as hemolytic anemia [...] TPI1 gene mutations lead to the production of unstable enzymes or enzymes with decreased activity. As a result, glycolysis is impaired and cells have a decreased supply of energy. Red blood cells depend solely on the breakdown of glucose for energy, and without functional glycolysis, red blood cells die earlier than normal. (emphasis mine)


Thus, since erythrocytes depend solely on glycolysis as energy source, there is a marked accumulation of DHAP toxic sub-products (Ahmed et al., 2003).

Sources:


Reference, G. (2017). triosephosphate isomerase deficiency. [online] Genetics Home Reference. Available at: https://ghr.nlm.nih.gov/condition/triosephosphate-isomerase-deficiency#genes [Accessed 16 Jul. 2017].
Ahmed, N., Battah, S., Karachalias, N., Babaei-Jadidi, R., Horányi, M., Baróti, K., Hollan, S. and Thornalley, P. (2003). Increased formation of methylglyoxal and protein glycation, oxidation and nitrosation in triosephosphate isomerase deficiency. Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease, 1639(2), pp.121-132.