Considering that C3 is a DEG and is present in the supernatants of chondrocyte cultures treated with the extract and that the extract proteases are able to directly cleave C3 and generate C3a (9), C3a fragments might bind to C3aR (also a DEG in our transcriptome analysis), activating nuclear factor kappa B (NF-κB) and the production of inflammatory cytokines, such as IL-6, and factors involved in angiogenesis, such as IL-8 and VEGF, thus resembling the events observed in joint diseases (Figure 6A). This evidence concerns the gene C3AR1 and arthropathy.