The lack of somatic genetic alterations other than CTNNB1 mutations and low levels of genomic complexity may provide an explanation for the indolent behavior of SPNs, akin to colorectal polyps associated with familial adenomatous polyposis in patients with germline APC mutations developing multiple KRAS wild‐type, benign tumors where a dysfunctional APC can be the only driver (Leoz et al., 2015; Takane et al., 2016). Here, APC is linked to Familial adenomatous polyposis.