A recent study has demonstrated that blocking a secondary bulge formation during hair growth induced defective HF regeneration and compromised long‐term maintenance of HFSCs.[8] They found the bulge formation was related to the suppression of OXPHOS and glutaminolysis by mTORC2‐Akt signaling, a critical metabolic event in regulating the transition between ORS cells and quiescent HFSCs.[8] Distinct from the defect in re‐establishing HFSC bulge in mice with mTORC2 deletion, Scd1−/− mice are lack of HFSC bulge formation in the first wave of hair growth during the postnatal period. Here, AKT1 is linked to hydrops fetalis.