Further, we realized that not only copy number amplification, but also copy number deletion events were more common in C2 and C3, compared to C1; the C3 subtype was predominantly linked to the deletion of genes involved in tumour proliferation and DNA repair processes37-39, encompassing BCL10, CDKN2B, MUTYH, CDKN2C, BACH2, and RUNX1 (Fig. 5F). The gene discussed is RUNX1; the disease is neoplasm.