Several studies support the importance of BECN1 in Huntington's disease pathology, as overexpression of it can slow the progression of Huntington's disease pathology in both cell and mouse models by inducing autophagy, while the expression of BECN1 in the brains of Huntington's disease patients declines with age.6,7,48,49 The downregulation of BECN1, as well as the other alterations in the CAMKK-AMPK signalling pathway, suggests that autophagy activity may be impaired in HD-iNs. This evidence concerns the gene BECN1 and juvenile Huntington disease.