In particular, the observation that only secretomes from metastatic cells both sustain CD73 and decrease TNFα expression in the lung (Figure 1C), while also preferentially functioning to increase the inflammatory state of macrophages in the absence of MSCs in vitro (Figure 3B and Supplementary Figure 2A), suggests that secreted factors from the primary tumor may function to recruit and reprogram MSCs toward an anti-inflammatory state within the premetastatic niche. Here, NT5E is linked to neoplasm.