In the murine B-cell neoplasms example, the cases with chromatin-modifying gene CREBBP or EP300 mutations that had a decreased H3K27 acetylation led to higher M2 polarization and a faster tumor progression when compared to CREBBP/EP300 wild-type, regulated via the FBXW7-NOTCH-CCL2/CSF1 axis [73]. The gene discussed is CREBBP; the disease is neoplasm.