HDAC2 silencing by enzymatic inhibition has a substantial impact on leukemia cell proliferation and immune regulation, as described in our previous work 10, where we established an HDAC2‐knockdown AML clone to better understand the role of cancer cell proliferation dynamics with and without treatment with the well‐studied HDAC inhibitors (HDACi) suberanilohydroxamic acid (SAHA) and entinostat (also known as MS‐275). Here, HDAC2 is linked to cancer.