In detail, we observed (a) more homogenous staining of E‐cadherin/β‐catenin and lower proliferation rates according to tumor specimens, (b) a biomarker‐dependent apoptosis induction and proliferation reduction by the EGFR inhibitor Gef, and (c) in contrast to other preclinical findings, a reduced response upon HSP90 inhibitor treatment in KRAS‐mutated tumor cells, which matches observations from clinical studies. The gene discussed is HSP90AA1; the disease is neoplasm.