Moreover, these cells showed increased R-loop formation, phosphorylation of replication protein A 32 (RPA32) at serine 4 and 8 residues—a marker of fork collapse [55]—and γ-H2AX signals (Fig. 8B, C), which confirmed that increased R-loop and DNA damage from DDX41 inhibition observed in cancer cell lines also occurred in primary immature hematopoietic cells. The gene discussed is H2AX; the disease is cancer.