The presence of both the tumor mutational signatures SBS3 and ID6 at high levels (> 50%), which is associated with HRD, and the absence of serrated pathway molecular characteristics, namely the BRAF p.V600E mutation and CIMP-high, suggests that tumorigenesis for the CRC from person 009 was driven by HRD deficiency related to BRCA1 inactivation. Here, BRAF is linked to neoplasm.