Abstract Proliferative glomerulonephritis (GN) is a critical condition in many forms of kidney diseases and characterized by the proliferation of mesangial cells with influx of inflammatory cells. Receptor tyrosine kinase Axl belongs to the TAM family, along with Mer and Tyro-3. Receptors from this family contribute to clearance of apoptotic cells and suppression of inflammation. Previously, we reported an important role of Axl-mediated mesangial proliferation in the anti-GBM induced mouse model of lupus nephritis. In this study, we investigated the signaling cascade induced by Axl activation in renal mesangial cells. We found that Axl activation led to the phosphorylation of mTORC1 complex, proceeded with the ribosomal protein S6 activation. Inhibition of NFκ-B activity diminished mTOR phosphorylation in mesangial cells, indicating that NFκ-B is a critical regulator for mTORC1 activation in the Axl/Akt pathway. Axl expression also participated in mesangial cell efferocytosis. Interestingly, mesangial efferocytosis is not mediated by Mer receptor tyrosine kinase, the canonical TAM family receptor facilitating apoptotic cell engulfment in macrophages. Taken together, data suggest that Axl mediated mTOR activation and apoptotic cell engulfment is renal mesangial cell specific, as those functions were not observed in similarly treated peritoneal macrophages.