HDAC5 and neoplasm: In a study exploring whether the TME was the cause of therapy resistance in PDAC, HDAC5 (Histone Deacetylase 5) was found to enable KRAS-independent growth by altering the TME myeloid cell composition, through the recruitment of tumor-associated macrophages (TAMs) via the HDAC5-CCL2 axis, with several potential drug targets [53].