In agreement with the high efficiency of HCI‐2509 treatment, regardless of the tumor‐driving EGFR or KRAS mutation, phosphorylation profiling revealed that HCI‐2509 treatment leads to less activation of the EGFR pathway by impeding the phosphorylation of Akt and the KRAS downstream targets, MEK and ERK. This evidence concerns the gene KRAS and neoplasm.