Within the human body, billions of cells undergo apoptosis daily, and it is important that these cells are efficiently removed without causing an inflammatory response. This is mainly carried out by innate immune cells, such as macrophages, in a process referred to as efferocytosis. During efferocytosis, apoptotic cells attract macrophages via 'find-me' signals exposed on their cell surface and trigger phagocytosis via 'eat-me' signals. Following uptake and digestion, macrophages undergo extensive reprogramming towards a pro-resolving phenotype that promotes tissue repair. To date, no study has investigated these reprogramming events on the proteome level, and so in order to differentiate between the proteomes of the macrophage and apoptotic cell, we employed stable isotope labeling by amino acids in cell culture (SILAC). We show that using this approach, we can successfully dissect the mixed proteomes and successfully map the reprogramming events in macrophages following efferocytosis. Specifically, we show that these cells adopt a unique pro-resolving phenotype underpinned by an increase in efferocytic and anti-inflammatory markers. Notably, we also show that the secretome of efferocytic macrophages can alter the phenotype of naive macrophages, shifting them towards an efferocytosis-like phenotype. These results have important implications for clinical aspects of efferocytosis, specifically in cases where we can map macrophage reprogramming in disease states.