Human tumor sequencing data reveals a substantial co-occurrence of mutations between DDR1 and either RUNX1 or CBFβ, whereas such co-occurrence is not necessarily observed between RUNX1 and CBFβ. These data are in line with our findings, as mutations to DDR1 and either RUNX1 or CBFβ would have two distinct effects, while loss of both RUNX1 and CBFβ would be largely redundant. Here, DDR1 is linked to neoplasm.