This study reports a novel form of non-Mendelian inheritance in mice, where an epigenetic change in the *Kit* gene is inherited from both male and female parents. The *Kit* gene, which plays a crucial role in several developmental processes, is normally silent in the haploid phase. However, in heterozygotes carrying a null mutant *Kit*^*tm1Alf*^ allele, the offspring exhibit a white-spotted phenotype characteristic of *Kit* mutants, despite being genetically wild type. This phenomenon, termed "paramutation," is caused by a decrease in Kit mRNA levels and the accumulation of non-polyadenylated RNA molecules of abnormal sizes. These abnormal RNA molecules are present in spermatozoa and can be inherited through microinjection into fertilized eggs, leading to a heritable white tail phenotype. The study identifies an unexpected mode of epigenetic inheritance involving the zygotic transfer of RNA molecules, providing insights into the molecular mechanisms underlying paramutation.This study reports a novel form of non-Mendelian inheritance in mice, where an epigenetic change in the *Kit* gene is inherited from both male and female parents. The *Kit* gene, which plays a crucial role in several developmental processes, is normally silent in the haploid phase. However, in heterozygotes carrying a null mutant *Kit*^*tm1Alf*^ allele, the offspring exhibit a white-spotted phenotype characteristic of *Kit* mutants, despite being genetically wild type. This phenomenon, termed "paramutation," is caused by a decrease in Kit mRNA levels and the accumulation of non-polyadenylated RNA molecules of abnormal sizes. These abnormal RNA molecules are present in spermatozoa and can be inherited through microinjection into fertilized eggs, leading to a heritable white tail phenotype. The study identifies an unexpected mode of epigenetic inheritance involving the zygotic transfer of RNA molecules, providing insights into the molecular mechanisms underlying paramutation.