Rather, it is most decidedly due to its ability to simultaneously act on well-characterized cancer cell-intrinsic growth-promoting pathways, such as the MYC pathway active in TNBC86, the mechanisms that control S100A8/A9 expression in multiple cell types in the TME, and yet-to-be-explored mechanisms by which PIM may control expression or secretion of additional cytokines and chemokines critical for recruiting various immunosuppressive myeloid cell types (Figs. 5g, h, and 6). Here, IGKV1D-22 is linked to cancer.