CaMKK2 is a key regulator of cellular and whole‐body energy metabolism which protects cells from ferroptosis in melanoma,[31] regulates mitochondrial function,[32] and is upregulated in hepatocellular carcinoma and prostate cancer.[33, 34] Previous studies on CSCs have reported the importance of mitochondrial function in the alteration of CSC fate.[35, 36, 37, 38] In present study, we found that CaMKK2 was also upregulated in lung CSCs and bulk tumor cells, and TIPRL depletion allowed PP2Ac to bind to the C‐terminal region of CaMKK2, leading to inactivation of the CaMKK2 signaling pathway. Here, CAMKK2 is linked to neoplasm.