Similarly to our results, those authors concluded “that PGRMC1 is able to suppress broad networks necessary for multi-lineage fate specification.” Our hypothesis suggests that PGRMC1 Y180 phosphorylation and PI3K/AKT activity could be associated with elevated GSK-3β Ser9 phosphorylation and β-catenin signaling as observed in in some cancers [47]. The gene discussed is AKT1; the disease is cancer.