Abstract
Histone deacetylase 10 (HDAC10) is emerging as a critical modulator of tumor immunity, chemoresistance, and transcriptional plasticity in colorectal cancer. Its suppression has been linked to altered CD8(+) T cell activity, increased p53 expression, and reduced programmed death ligand 1 levels, suggesting a potential role in immune evasion. However, mechanistic understanding of HDAC10's selective function, especially in shaping the tumor microenvironment, remains limited. We advocate for targeted investigations using isoform-selective inhibitors, functional in vivo studies, and immune subset profiling to clarify HDAC10's therapeutic relevance in colorectal cancer.