The in vitro cell and in vivo xenograft tumour models demonstrated that [1] cells expressing CHK2T68D grown as tumour spheres or xenograft tumours were less sensitive to oxaliplatin and [2] treatment with BML-277 suppressed OR cells grown as colonies, tumour spheres, and xenograft tumours, supporting the idea that the activation of CHK2 signalling is critical for overcoming oxaliplatin and is associated with the development of oxaliplatin resistance in colorectal cancer. This evidence concerns the gene CHEK2 and neoplasm.