Regarding the possible molecular mechanisms underlying this effect, our results suggest that BRCA1 mutations could influence cell cycle transition and tumor immunomodulation through the p53 or JAK–STAT pathway, whereas BRCA2 mutations could influence cell cycle transition, tumor immunomodulation cell migration, and energy metabolic processes via PPAR signaling, AMPK signaling, p53 signaling, the JAK–STAT pathway, the NF-κB pathway, and the regulation of cell adhesion molecule interactions. This evidence concerns the gene SOAT1 and neoplasm.