Figure 1: The somatic strand-specific imprinting and segregation (SSIS) model: The SSIS model was proposed to produce developmentally nonequivalent daughter cells of the cerebral hemisphere laterality generating progenitor cell in embryogenesis. One of the daughter cells, the one placed on the left side of the embryo (with respect to anterior-posterior and dorso-ventral axes), inherits specific chromatids of both homologs of Chromosome 11, those containing the template “Watson” (W) strand with the expressed (ON) epiallele of the hypothetical language-process specifying gene (DOH1) gene. The daughter cell on the right side of the embryo inherits indicated chromatids/strands with epigenetically silenced DOH1 gene’s epialleles. A hypothetical RGHT1 (righthandedness- specifying gene) directs biased segregation of differentiated sister chromatids by functioning at the Chr. 11 centromere. The DNA strands are color-coded to indicate their biased distribution to specific daughter cells. Grey colored strands reflect “younger” strands synthesized in the parental cell. Due to biased strands “W,W::C,C” segregation occurring in mitosis, differentiated daughter cells result through asymmetric cell division, and after subsequent growth, differentiated brain hemispheres develop such that a person processes language in the left hemisphere of the brain. In contrast, homozygous individuals containing the nonfunctional allele of the RGHT1 gene, r/r (r for random), lack biased segregation and therefore exhibit random hemispheric asymmetry distribution. It is suggested that predisposition to breast cancer only in a minority of r/r individuals results from stochastic errors of the SSIS process in breast tissue stem cells, including allowing rare somatic recombination events to cause loss-of-heterozygosity of imprints of tumor suppressor genes.