As regards the first described mechanism, the decrease in progesterone receptors of both types and total decidual progesterone receptor levels in placental abruption or after THR treating was actually confirmed by Lockwood et al. (2012) and Nishimura et al. (2020) [50,54] The responsibility for this decrease was assigned to THR in the mechanism of ERK1/2 MAPK phosphorylation, with p38 MAPK or p65 NF-κB pathways probably remaining uninvolved [50]. The gene discussed is MAPK3; the disease is placental abruption.