Co-segregation of the variants with colorectal cancer and/or polyps, in-silico modeling, and two hit inactivation by loss of heterozygosity or somatic point mutations in tumors, together with the absence of other possible predisposing variants by exome sequencing, supported the idea of tumor predisposition being attributable to the BMPR1A variants. Here, BMPR1A is linked to colorectal cancer.