We further investigated the pathways associated with these genes using Ingenuity Pathway Analysis (IPA; p < 0.05) and identified diverse pathways for each tissue sample with only three pathways (apelin cardiomyocyte signaling pathway, calcium signaling, Huntington’s disease signaling) showing an overlap (Supplementary dataset 8: IPA_splicing.xlsx); this indicates that under mutant FUS (ΔNLS-FUS) overexpression, aberrant splicing regulation varies and is tissue-dependent. Here, APLN is linked to juvenile Huntington disease.