At the intracellular level, three main pro-inflammatory signaling kinase cascades responding to soluble mediators are involved in RA, all being influenced by microalgal metabolites: the Nuclear Factor Kappa-Β (NF-kB)-mediated pathway [30], the Janus kinase 2/Signal Transducers and Activators of Transcription 3 (JAK2/STAT3) pathway [31], and the Jun N-terminal kinase (JNK)/p38 Mitogen-Activated Protein Kinase (p38 MAPK) pathway [32], the latter being predominant in the lining layer and endothelial cells. The gene discussed is STAT3; the disease is rheumatoid arthritis.