To the Editor,

We read the publication on “Transforming growth factor beta (TGFβ) receptor II (TGFBR2) promoter region polymorphism in Brazilian breast cancer (BC) patients: association with susceptibility, clinicopathological features, and interaction with TGFB1 haplotypes.” with a great interest [1]. Vitiello et al. concluded that G-875A is a protective factor against BC, especially from luminal-A subtype, but may promote anaplasia in established tumors, consistent with TGFβ signaling roles in BC [1]. Indeed, the effect of genetic factor on BC is possible. The identified effect of G-875A might be modified by other genetic and non-genetic factor; therefore, the confounding effect of TGFβ1can be expected. Nevertheless, the isolated effect of G-875A polymorphism might be explainable via molecular change analysis. Based on the quantum molecular calculation technique as presented in the previous reports [2,3,4], the molecular weight change due to G-875A polymorphism is equal to − 16 g/Mol (151.13 g/Mol to 135.13 g/Mol). Similar to the described pathogenesis in other medical disorders [2,3,4], the G-875A variant will result in a less expression of TGFBR2, which further imply a less amount of growth factor to stimulating BC carcinogenesis. This result is concordant with the previous report by Barlow et al. that a higher expression of TGFBR2 is associated with a poorer prognosis of breast tumor [5].