Paulus et al. proposes a mechanism that lends credence to this notion by indicating that the concurrent existence of conditions such as T2DM, obesity, arterial hypertension, and pulmonary disease is responsible for inducing a systemic proinflammatory state (Figure 1B), characterized by elevated levels of tumor necrosis factor (TNF)-α, interleukin (IL)-6, and IL-1ß, amongst many others (Van Linthout and Tschöpe, 2017). The gene discussed is TNF; the disease is obesity disorder.