GTPBP2 and renal tubular dysgenesis of genetic origin: Based on the observation that GAAC activation in mice attenuates the growth defects caused by the combination of reduced tRNAArg(UCU) levels and a defect in the ribosome recycling component GTPBP2 [86], we speculate that GAAC activation by reduced tRNA function in mammals will likewise attenuate RTD and promote survival.