Last, but not least, it should be kept in mind when using patient-derived hiPSCs that additional mutations in other genes or in HNF4A regulatory regions could also modulate the outcome of the in vitro differentiation experiments, as illustrated above for GATA6. To conclude, additional studies are necessary to address how HNF4A mutations cause MODY in humans, especially using the next generation of pancreatic differentiation protocols that improve the production of fully mature β-like cells. The gene discussed is HNF4A; the disease is MODY.