Maternal thyroid hormones [THs; 3,5,3'-triiodothyronine (T3) and thyroxine (T4)] show central roles in the fetal and neonatal development during the gestation and lactation periods (El-bakry et al., 2010; Ahmed, 2011, 2012a,b, 2013, 2014, 2015a-c, 2016a-d, 2017a-v, 2018a-r; Ahmed and Ahmed, 2012; Ahmed et al., 2008; 2010; 2012; 2013a,b, 2014, 2015a,b, 2018a,b; Ahmed and Incerpi, 2013; Van Herck et al., 2013; Ahmed and El-Gareib, 2014, Incerpi et al., 2014; Candelotti et al., 2015; De Vito et al., 2015; El-Ghareeb et al., 2016; Ahmed and El-Gareib, 2017), in particular the hematopoietic cell proliferation and growth, the number of red blood cells (RBCs) and white blood cells (WBCs), and platelet counts (Grymula et al., 2007; Kawa et al., 2010; Pascual and Aranda, 2013; Kandir and Keskin, 2016). In the bone marrow, Kendrick et al. (2008) reported that THs can induce its cellular production. In human early hematopoietic cells, THs might play a significant action in the regulation of the growth (Gruber et al., 1999; Grymula et al., 2007; Kawa et al., 2010). More importantly, the genomic and nongenomic actions of THs might be regulated these mechanisms (Gruber et al., 1999; Milne et al., 1999; Dorshkind and Horseman, 2000; Porter and Mandel, 2000; Bauer et al., 2001; Omazic et al., 2001; Marongiu et al., 2004; Kawa et al., 2010; Barreiro Arcos et al., 2011; Franchini et al., 2011; Kandir and Keskin, 2016). In addition, Kawa et al. (2010) reported that any change in the gene expressions of thyroid receptors (TRs; α and β) might change the hematopoietic progenitors.