ACTA1 and lung adenocarcinoma: RNA quantification revealed significant downregulation of CNPY2 after inhaled miR‐30a treatments and protein analysis confirmed decreased CNPY2 expression, as well as downstream PERK/DDIT3 signaling.[46] The miR‐30a‐3p was previously identified as a key regulator of the oncogene CNPY2 and inhibited epithelial‐mesenchymal transition (EMT) in human lung adenocarcinoma.[47] Similarly, miR‐30a treatments suppressed EMT away from the α‐SMA+ myofibroblast signature by downregulating N‐cadherin relative to E‐cadherin.