Considering that Type 2 DM is a protein misfolding disorder [55], another possible explanation could be that the increase in Cav1.4/cacna1f transcription may have resulted in misfolding of the protein product, such that it could have been misassembled, resulting in accumulation of immature synaptic ribbons or that it could have been rendered undetectable by inaccessibility of the epitope in the misfolded protein. This evidence concerns the gene CACNA1F and proteostasis deficiencies.