NID2 and craniofacial microsomia: The “laminin-interaction” signaling pathway was predicted to be most frequently disrupted in the present cohort of patients with HFM, predominantly by mutations in ITGB4, NID2, or LAMA5. This is consistent with the fact that previous reports have demonstrated a close relationship (either positive or negative) between laminin interaction and bone formation during both osteogenesis and osteoclastogenesis (Langen et al., 2017; Susek et al., 2018).