In parallel, we recently pinned mutant KRAS as a molecular determinant of the propensity of pleural-metastasized tumor cells for MPE formation: mutant KRAS delivered its pro-MPE effects by directly promoting C-C chemokine motif ligand 2 (CCL2) secretion by pleural tumor cells, resulting in pleural accumulation of MPE-fostering myeloid cells11. The gene discussed is KRAS; the disease is pleural neoplasm.