Similar observations come from works in a Huntington's disease (HD) mouse model, in which mutated Htt (the gene of HUNTINGTIN protein) is able to block mitochondrial movement [71] and causes a redistribution of kinesin and dynein in primary cortical neurons [72]; in Parkinson disease (PD) cellular and mouse models where PINK1 has been shown to interact with MIRO and MILTON [73], as well as with α-SYNUCLEIN, LRRK2, and PARKIN, to disrupt the microtubule network in the cell [74–76]. This evidence concerns the gene HTT and Huntington disease.