However, when we challenged cells to induce additional replication stress, either by treatment with the DNA polymerase inhibitor Aphidicolin (Fig. 3B) or by expressing the c-MYC oncogene (Fig. 3C), H4K16ac-depleted HME1s exhibited compromised fitness, mirroring the synthetic lethal phenotype observed in genomically unstable cancer cells (Fig. 3C) [7]. This evidence concerns the gene MYC and cancer.