The reason is that genetic or pharmacological targeting of the oncogenic MUC1 subunit MUC1-C enhances the transcription rate of the immune checkpoint ligand PD-L1 in triple-negative breast cancer (TNBC) cells by recruiting MYC and NF-kB p65, which in turn inhibits PD-L1 expression [92]. Here, MUC1 is linked to triple-negative breast carcinoma.