The phenotypes of double mutant mice whose genomes are homozygous for an <i>Mbp</i> (myelin basic protein) mutation and hemizygous for a juvenile-lethal <i>Plp</i> (proteolipid protein) mutation were compared in earlier studies. The results suggested that the shiverer <i>Mpb</i> mutation might have some unexplained ability to partially rescue oligodendrocytes (OLs) from the ‘death sentence’ that is imposed by the <i>Plp</i> mutations. Conversely, they also indicated that the juvenile-lethal <i>Plp</i> mutations may normalize shiverer OL morphology by reducing the numbers of microprocesses. The <i>Plp</i> mutation rumpshaker produces a mild hypomyelination without reduction in OL numbers and a normal lifespan. This report describes double mutant mice combining two <i>Mbp</i> mutations with rumpshaker, utilizing a common B6C3F1 hybrid-based genetic background. Initial studies on B6C3F1 rumpshaker optic nerve and spinal cord white matter showed unanticipated signs of OL death, with morphologic criteria suggestive of an apoptotic mechanism. In shiverer*rumpshaker double mutant mice, this small class of dying cells could not be identified. White matter morphology was similar to that of mice expressing only the shiverer mutation, except that OL microprocesses were far less abundant. This evidence suggests that, despite their distinctive phenotypic differences, rumpshaker may share more characteristics with the juvenile-lethal <i>Plp</i> mutations than has previously been recognized.