As noted in the Background section, whereas Akita islets synthesize approximately one third of their proinsulin as the mutant protein [14], transgenic hProC(A7)Y-CpepGFP mice express lower levels of Akita-like mutant proinsulin that only modestly lowers intra-islet insulin levels and results only in prediabetes — expression of the transgene in Ins2+/− and Ins2−/− genetic backgrounds [23] increases the severity of the diabetes phenotype [16]. The gene discussed is INS; the disease is diabetes mellitus.