Prior studies have reported rare ALK rearrangement events in PSC patients, but heterogenous expression of ALK fusions in 2–7% of lung adenocarcinoma with multiple potential breakpoints in EML4, and alternate canonical or non‐canonical fusion partners involving KIF5B, ASXL2, ATP6V1B1, PRKAR1A, and SPDYA [49, 50]. This evidence concerns the gene PRKAR1A and lung adenocarcinoma.