suggested that RGS1 is upregulated by IFN/STAT1 path, and weaken trafficking of circulating T cells to tumors by suppressing calcium influx and inhibiting activation of the ERK and AKT kinases; conversely, its knockdown in adoptively transferred tumor-specific CTLs remarkedly increase their infiltration and productively suppress tumor growth in lung and breast tumor grafts in vivo, which is further improved when combined with PD-L1 checkpoint inhibition (56); and, RGS1 is a novel marker and promoting factor for CD8+ T-cell exhaustion (57). This evidence concerns the gene STAT1 and breast neoplasm.