While stiff EVs appear to downregulate immune signaling from resident fibroblasts in the lung via a decrease in expression in S100A4, S100A6, S100A12, and S100A13 to potentially to aid cancer cells in evading immune detection, the soft EVs demonstrate the ability to upregulate expression of cancer-associated fibroblast (CAF) markers (ACTA2, COL1A1, VIM) while also presenting increased inflammatory capacity (elevated S100A10, S100A16) in the resident fibroblasts. The gene discussed is S100A16; the disease is cancer.