NFKB1 and neoplasm: Consistent with the hypothesis that MLCs promote and sustain an inflammatory microenvironment through IL-6, CSF, and CD44 signaling, which results in the accumulation of tumor-infiltrating microglia and the activation of NFκB signaling in the tumor cells, the inferred abundance of MLCs was strongly correlated with the expression of IL-6/STAT3, TNF-α, TGF-β, mTORC1, and NFκB signaling gene sets in this cohort, as well as with the abundance of microglia (Spearman’s correlation between MLC and microglia abundance r = 0.70, FDR < 0.001).