Furthermore, other findings here showing that patient-derived anti-GRP78 autoantibodies activate monocyte-lineage phagocytes, and enhance their productions of injurious mediators that are implicated in the genesis of emphysema and osteoporosis are direct evidences of deleterious autoantibody effects [11], [12], [27]–[29]. This evidence concerns the gene HSPA5 and pulmonary emphysema.