We suspect that GATA3 recruits UTX/MLL4, allowing them to function in a coordinated manner, either simultaneously or sequentially methylating H3K4 and demethylating H3K27, to broadly maintain increased level of H3K4me337 and decreased level of H3K27me2/3 at the target promoters, thereby transcriptionally activating tumor suppressor genes such as UTX or Dicer and inhibiting the progression of breast cancer. The gene discussed is DICER1; the disease is breast carcinoma.