KRAS and neoplasm: We propose that the persistent high expression of SIAH (SIAHHigh/ON) post-NACT/NST reflects tumor-driving EGFR/K-RAS/MAPK pathway activation (ON), resulting in tumor progression, immuno-suppression, and chemo-resistance, versus the loss of SIAH expression (SIAHLow/OFF) post-NACT/NST reflects this tumor-driving pathway is inactivated (OFF), resulting in tumor regression, immune responsiveness, and chemo-sensitivity[3,76].