Our data are consistent with such a role for VGLL3 both in relation to myofibroblast function and collagen I expression, as well as development of Endo-MTs, raising the intriguing possibility that VGLL3 may contribute to the female bias in SSc through its modulation on Hippo-TEAD signaling in myofibroblasts or EndoMTs, or both. Here, VGLL3 is linked to systemic sclerosis.