In CRC patient tumor genomic data, we were able to detect a trend toward a mutually exclusive interaction between ARID1A and rare baseline EGFR amplifications, as well as significant mutually exclusive interactions between ARID1A and BRAF and KRAS, two genes that are downstream of EGFR signaling and known to confer resistance to anti-EGFR therapy. The gene discussed is KRAS; the disease is neoplasm.