Only 2 of 5 (40%) ERBB2 amplified CRC patients displayed concurrent oncogenic alterations; the first patient displayed multiple subclonal driver variants (BRAF V600E, KRAS Q61H, and a CCDC6-RET fusion) as well as EGFR ectodomain mutations (G465R, S464L) suggestive of the acquisition of several on- and off-target resistance mutations in response to standard-of-care cetuximab therapy while the second patient had a co-occurring subclonal KRAS G12R mutation (Figure 5, Supplementary Table 2). The gene discussed is KRAS; the disease is colorectal carcinoma.