We can speculate that the reduced level of expression of GIPR vs GLP-1R in beta cells under normal conditions might result in the selective preservation of GLP-1 responses in a context where expression of both receptors is compromised; alternatively, as our results point to a higher reliance on signal amplification mechanisms for the GIPR, it is possible that beta cell GIP responses are more dependent on conservation of downstream signaling mechanisms that might become dysfunctional in T2D. The gene discussed is GLP1R; the disease is type 2 diabetes mellitus.