This inflammatory status can promote carcinogenesis by enabling cell proliferation, apoptosis, and angiogenesis,5 impaired insulin signaling (thereby inducing hyperinsulinemia),6 disturbed bioavailable sex steroid hormone levels through enhanced aromatase expression,7 and downregulating of sex hormone‐binding globulin (SHBG) production.8 Here, INS is linked to hyperinsulinism.