We interpret each distribution as a measure of the plausibility that a given combination of changes in c1, Tref, and rendo reproduces the development of the HF phenotypes, starting from the healthy configuration, either in the presence (Fig. 5, a1–a6) or absence (Fig. 5, b1–b6) of doxorubicin exposure. The gene discussed is ETV7; the disease is hydrops fetalis.