Specifically, mutant KRAS tumor cells were shown to respond to IL-1β secretion from the CCL2-recruited myeloid cells by activating the alternative signaling cascade of NF-κB pathway, forming in this way a circuit which fuels the secretion of CXCL1 by tumor cells, enhances tumor and MPE development and drives drug resistance [25]. This evidence concerns the gene KRAS and neoplasm.