Thus, as opposed to the increase in MHC-I expression in response to ET and IFNγ stimulation that is, at least in part, a cell-intrinsic effect and observed in the breast cancer cells in 2D culture, the effect of ET on STING expression is likely not cell intrinsic, but rather dependent on a more complex interplay between the cancer cells and the TME. The gene discussed is STING1; the disease is breast carcinoma.