Thus, through this and other mechanisms, mHtt may affect nuclear and cytoplasmic proteins that regulate transcription factors (e.g. CBP, REST), survival/neurogenesis/apoptosis signalling (e.g. Akt, EGF, p53), mitochondrial function, tumour suppression, vesicle release (e.g., brain-derived neurotrophic factor (BDNF) vesicles), proteolysis (caspases and calpain), protein degradation (ubiquitin-proteasome system), neurotransmissors and axonal transport [28,69,70,71,72,73,74,75,76,77,78,79,80]. This evidence concerns the gene BDNF and neoplasm.