DLK1 and neoplasm: Furthermore, consistent with the broadly known well-knit interaction between the cellular and biochemical components of the inflammatory cascade [17,27,41], we also demonstrated that concomitant with documented enhancement of M1 polarization at the expense of a depleted M2 pool, PG2 markedly represses the tumor-promoting effects of anti-inflammatory cytokines and inhibits the NSCLC stem cell-like phenotypes induced by M2-conditioned medium (Figure 3 and Figure 4).