To date, several studies identified genetic modifiers of AAO in HD participating in glutamatergic transmission (GRIK2, GRIN2A, GRIN2B) [8]–[11], axonal trafficking (HAP1) [12], gene transcription (TCERG1, TP53) [13], [14], energy metabolism (PPARGC1A) [15]–[17] or protein degradation (UCHL1, ATG7) [18]–[20] representing various intracellular pathways involved in pathogenic processes of HD [21]. This evidence concerns the gene TP53 and Huntington disease.