However, in uncontrolled metastatic tumors, MYC was downregulated, but STAT5A/B was expressed, suggesting that MYC-dependent STAT5A/B-PD-L1 was controlled in the primary and metastatic tumors where our novel approach worked, whereas the nonresponsive metastatic lesions were governed by MYC-independent STAT5A/B interaction. This evidence concerns the gene STAT5A and metastatic neoplasm.