MERTK and neoplasm: Enhanced TAM receptor signaling in response to PtdSer expressed on apoptotic cells resulted in AKT-dependent PD-L1 expression on tumor cells and macrophages, and MERTK inhibition by genetic deletion or treatment with MERTK inhibitor MRX-2843 led to decreased expression of PD-L1 on tumor cells and innate immune cells [170].