F8A1 and Huntington disease: Given the above findings, especially that HAP40 relies on HTT for its protein stability and that it binds wildtype and mutant HTT with similar affinity, and also considering that mutant HTT protein exists at similar or even lower levels as that of normal HTT in tissues from HD patients and multiple mouse models of HD [46, 47], one can speculate that the levels of HAP40 protein should not change significantly by HD mutations, a conclusion that would contradict with the early report of elevated HAP40 levels in HD cells and tissues [35].