Within metastatic niches, host−derived growth factors robustly activate ERK signaling and increase anti−apoptotic MCL1 in osteosarcoma cells, supporting survival during lung colonization; this situates neurotrophin−responsive MAPK signaling within a broader growth−factor ecosystem and underscores that intercepting ERK−driven programs can influence both tumor persistence and the composition of immune infiltrates that are conditioned by MAPK activity (48–50). The gene discussed is MCL1; the disease is neoplasm.