Functional assays further showed that PART1 knockdown‐mediated anti‐proliferation, anti‐migration, and anti‐invasion effects were suppressed via JAK1 or JAK3 overexpression in NSCLC, in line with that of Wang et al49 Further xenograft tumor growth model of NSCLC also confirmed the antitumor genesis role of PART1 knocking down via inactivation of JAK‐STAT signaling pathway. The gene discussed is JAK3; the disease is non-small cell lung carcinoma.