Calibrated gel filtration, molecular dynamics (MD) simulation, hydrogen–deuterium exchange mass spectrometry (HDX-MS), diffusion-ordered (DOSY) NMR, (soft-ionizing) nano-LC MS, and X-ray crystallography (see below) all confirmed that neither (mild) acidosis nor the hitherto investigated disease-causing homodimerization surface mutations led to monomerization of the E3 dimer [24, 25, 30, 59–62]. The gene discussed is DLD; the disease is Acidosis.