In recent years, efforts have been made to exploit TNBC unique immunobiology—including its relatively high tumor mutational burden (TMB) [18], PD-L1 expression [11,19], and abundance of tumor-infiltrating lymphocytes (TILs) [20,21]—to develop strategies that convert “cold” tumors into “hot,” actionable immunotherapeutic targets. The gene discussed is CD274; the disease is neoplasm.