In acute myeloid leukemia, exosomal miR-34a targets histone deacetylase 2 (HDAC2), affecting leukemia stem cell survival and exosome shedding, illustrating potential therapeutic avenues.[142] Similarly, in gastric cancer, exosomal LINC00355 modulates HDAC3 activity, inhibiting TP53INP1 transcription and enhancing epithelial-mesenchymal transition and cancer progression.[143] These studies underscore the intricate dynamics between exosomes and epigenetic regulators in pathological states, suggesting avenues for future cardiac hypertrophy research. This evidence concerns the gene HDAC2 and gastric cancer.