These earlier patient studies and mouse and zebrafish genetic models of BS all point to an association between lack of hydroxylysine aldehyde cross‐linking in bone collagen and bone fragility.(17, 18, 24, 25, 26) In a Plod2 knockout zebrafish model, telopeptide lysine hydroxylation was blocked and collagen type I was more extractable from bone consistent with a decrease in stable cross‐links.(24) This implies that altered collagen cross‐linking might more generally contribute to bone fragility in OI and other conditions. Here, PLOD2 is linked to Bloom syndrome.