For example, HFD mice have insulin resistance and exhibit hyperinsulinemia with a high level of circulating insulin, a well‐known myoblast proliferation and differentiation enhancer (Allen & Rankin, 1990; Brown et al., 2016; Prentki & Nolan, 2006), which may boost SC function and thus compensate HFD‐caused SC harm in vivo, at least in a temporary manner. The gene discussed is INS; the disease is hyperinsulinism.