While total protein levels and processing of proSP-C(I73T) were not consistently altered, perhaps related to the nature and proteostasis status of the cells, our work supports the concept that altering SP-C(I73T) trafficking route by EMC3/VCP inhibition is sufficient to minimize damage to AT2 cells and thus to ameliorate ILD. The gene discussed is SFTPC; the disease is interstitial lung disease.