In our analyses, BMS354825 suppressed the viability of AGS cells without CRKL amplification as well as the viability of MKN74 cells with CRKL amplification, suggesting that a CRKL-independent pathway, which has been previously implicated [36], may also be involved in the BMS354825-mediated cytotoxicity seen in gastric cancers. The gene discussed is CRKL; the disease is gastric cancer.