Phf8 is also a mediator directly linking Hcy-thiolactone and N-Hcy-protein with dysregulated mTOR signaling and its downstream outcomes such as impaired autophagy flux and upregulated Aβ accumulation, thus supplying a plausible mechanism explaining neuropathy induced by Blmh deficiency [125] (Figure 6) and explaining an association of HHcy with Alzheimer’s disease [8]. This evidence concerns the gene BLMH and early-onset autosomal dominant Alzheimer disease.