In contrast, in the LDL_high group, SPP1+ macrophages and monocytes showed pronounced increases in both outgoing and incoming signaling strength (Figure 3E), indicating that these myeloid populations become more central hubs under high LDL conditions and cooperatively amplify the IL6, CSF, and TENASCIN axes to drive tumor growth, invasion, and immunosuppression. Here, SPP1 is linked to neoplasm.