Given that our data indicate that SOX4 and SMARCA4 are uniformly activated in basal-like breast tumors, our findings not only delineate a mechanism by which SOX4 and SMARCA4 mediate PI3K activity in TNBC or basal-like breast cancers but have also identified a novel complex by which SOX4 cooperates with SMARCA4 to modulate transcriptional activation and oncogenic signaling in basal-like breast cancer. Here, SMARCA4 is linked to breast neoplasm.