By leveraging the tumor-driving EGFR/K-RAS/SIAH pathway activation (ON)/inactivation (OFF) in TNBC, we hope to differentiate TNBC pIR patients by correlating SIAHHigh (high-risk) versus SIAHLow (low-risk) expression in residual tumors post-NACT/NST. This evidence concerns the gene KRAS and neoplasm.