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Mutations in <i>NRAS</i> constitutively activate cell proliferation signaling in malignant neoplasms, such as leukemia and melanoma, and the clarification of comprehensive downstream genes of <i>NRAS</i> might lead to the control of cell-proliferative signals of <i>NRAS</i>-driven cancers. We previously established that <i>NRAS</i> expression and proliferative activity can be controlled with doxycycline and named as THP-1 B11. Using a CRISPR activation library on THP-1 B11 cells with the <i>NRAS</i>-off state, survival clones were harvested, and 21 candidate genes were identified. By inducting each candidate guide RNA with the CRISPR activation system, <i>DOHH</i>, <i>HIST1H2AC</i>, <i>KRT32</i>, and <i>TAF6</i> showed higher cell-proliferative activity. The expression of <i>DOHH</i>, <i>HIST1H2AC,</i> and <i>TAF6</i> was definitely upregulated with <i>NRAS</i> expression. Furthermore, MEK inhibitors resulted in the decreased expression of DOHH, HIST1H2AC, and TAF6 proteins in parental THP-1 cells. The knockdown of <i>DOHH</i>, <i>HIST1H2AC</i>, and <i>TAF6</i> was found to reduce proliferation in THP-1 cells, indicating that they are involved in the downstream proliferation of <i>NRAS</i>. These molecules are expected to be new therapeutic targets for <i>NRAS</i>-mutant leukemia cells.