Our study suggests another novel mechanism where mutant p53 in stromal fibroblasts increases the level of secretory proteins such as SAAs (SAA1 and SAA2) and THBS4, triggering tumor-promoting pathways, including PI3K/AKT signaling, etc., in the mammary epithelial cells, which expedites the mammary tumor development. The gene discussed is SAA2; the disease is breast cancer.