Of note, we did not observe any differences in HDAC1 levels by comparing primary fibroblasts from RSTS patients to those from healthy donors,35 but clearly observed a decrease in the acetylation levels of histone residue H3K27, which suggests that there is no compensation for the lack of CBP/EP300 activity by reduction of HDAC1 levels or activities in RSTS cells. This evidence concerns the gene HDAC1 and Rubinstein-Taybi syndrome.