Late-stage CHF is characterized by constant activation of the immune system, in which adoptive Tregs (induced Tregs, iTregs) are activated and/or induced to proliferate by Kv1.3 channel activation, subsequently through autocrine secretion or paracrine secretion of predominantly TGF-β and to a much lesser extent IL-10 to stimulate cardiac fibroblast proliferation (cardiac fibrosis), thereby facilitating the progression to heart failure (Figure 9). Here, IL10 is linked to heart failure.