It has been reported that the progesterone receptor lacks the consensus sequence or half-sequence response element in the PRLR gene PIII promoter and demonstrated that progesterone induces an increase in PRLR mRNA in a non-classical manner by inducing the expression of PRLR through the cooperative activation of Sp1 and CEBPβ at the PIII promoter in mouse cells and T47D breast cancer cells (43). Here, PGR is linked to breast carcinoma.