Based on limited published evidence, CENATAC is a dual-function protein serving as a minor spliceosome component and centrosome regulator. It promotes splicing of AT-AN minor introns 1 and associates with the minor tri-snRNP complex 2. CENATAC negatively regulates centrosome duplication by modulating SASS6 degradation through acetylation-dependent mechanisms, with SIRT1-mediated deacetylation in G1 phase enabling SASS6 accumulation and procentriole assembly, while NAT10-mediated acetylation in mitosis promotes proteasomal degradation 3. Mutations in CENATAC cause mosaic variegated aneuploidy syndrome through excessive minor intron retention and chromosome 11 errors 1.