Based on this working hypothesis of the pathophysiology of lung fibrosis, the anti-inflammatory (inhibition of TNF-α, inhibition of monocytes, inhibition of neutrophil influx into the lung) and immune-modulatory (inhibition of IL-2, inhibition of T cells) characteristics of BI 1015550 can be expected to contribute to improvement of fibrosis, at least to some extent. Here, IL2 is linked to pulmonary fibrosis.