Normal inflammatory response represents the initial phase of the immune response. This normal or “good” inflammatory response is transient, followed by a return to the normal status. Dysregulated or “bad” inflammatory responses are observed in inflammatory, infectious diseases and cancers, and can be characterized by inappropriate levels of inflammatory markers, speed of generation, and major site of production, such as a vital organ. Chronic or smoldering inflammation is associated to cancer initiation as observed in lung, gut, or cervical cancers and with obesity, which is associated to multiple factors such as dysmetabolism, gut dysbiosis, immune dysfunction and immune exhaustion. Inflammation is also associated with cancer promotion, proliferation, metastasis, and thrombosis risks. Due to the persistent and high inflammatory response, immune tolerance is also amplified and leads to immune resistance. Thus, to amplify cancer cell control, the dynamics of the inflammatory response must be evaluated to determine its negative impact and to open a more personalized therapy including the return to a normal inflammatory/immune response. To optimize anti-IL6 therapies, we developed an algorithm to mathematically model inhibition of IL-6 activity in the presence of either siltuximab (anti-IL-6), tocilizumab (anti-IL-6R), or both. By analyzing data in COVID-19 cytokine storm, biological efficiency was not reached showing that there is a need to optimize anti-IL6/antiIL6R therapies which were not correctly used. We also retrospectively analyzed data from the randomized study with siltuximab in Castleman disease, and open new possibilities in cancer, particularly for immune therapies.