(42) demonstrated that the IL-6-dependent activation of STAT3 is required for satellite cell proliferation in response to muscle overloading. However, the relation between resistance exercise and IL-6-dependent activation of STAT3 for skeletal atrophy/hypertrophy should consider that IL-6-dependent activation of STAT3 linked to muscle hypertrophy in response to exercise is transient (40–42), while persistent increased IL-6 and STAT3 phosphorylation and activation are linked to muscle atrophy during pro-inflammatory conditions such as cancer cachexia (13–15, 17). This evidence concerns the gene STAT3 and cancer.