In the absence of RA, genetic depletion of CHAF1A blocked tumor growth (p < 0.0001, Figure 5j), supporting our previous findings.[26] Importantly, CHAF1A KD+RA phenocopied DFMO+RA and resulted again in a significant inhibition of tumor growth (p < 0.05) and induction of tumor apoptosis (p < 0.01) compared to single approach (Figure 5j). The gene discussed is CHAF1A; the disease is neoplasm.