The newly identified important mechanisms include, firstly, metabolic reprogramming with elevated nucleotide metabolism (via NME1) that allows the communication of tumor-stromal-immune cells through both outgoing (MIF-PLA2) and incoming (BAFF-TFRC) signals, all while being spatially colocalized with EGFR/hypoxia/MAPK/TGF-β pathways. The gene discussed is TNFSF13B; the disease is neoplasm.