In our LCMD RNA-Seq analyses, LOXL2 was the most highly expressed LOX/LOXL family member as well as the only LOX/LOXL member which correlated with PLOD2 expression, whilst in our previous work investigating collagen structure-function dysregulation in human lung fibrosis, we identified that gene expression of LOXL2 was significantly increased in IPF tissue when compared to age-matched control lung tissue (Jones et al., 2018). Here, PLOD2 is linked to idiopathic pulmonary fibrosis.