The concept of “actionable” somatic genomic alterations present in each tumor (e.g., point mutations, small insertions/deletions, and copy-number alterations that direct therapeutic options, obtained from systematic genomic profiling) has rarely been achieved beyond a limited number of oncogene point mutations, such as EGFR, KRAS, TP53, PIK3CA that are commonly shared by many patients and across many tumor types [48]. Here, KRAS is linked to neoplasm.