It is possible that when cardiomyocytes begin to suffer from increased after-load, cytokines, such as heparin-binding epidermal growth factor, act as an autocrine and local paracrine cardiac growth factor, thus resulting in the loss of gap junction proteins within a spatially confined microenvironment [34] and inducing the early stage of ventricular hypertrophy [28]. The gene discussed is EGF; the disease is Ventricular hypertrophy.