Generally, it seems that the tumor microenvironment helps activate cathepsins, which in turn activate oncogenesis: mutant HRAS in mammary epithelial cells upregulates CTSB and CTSL; the HER2 oncogene drives expression of CTSB through the transcription factor myeloid zinc finger 1 (MZF1), and CTSB is a functional driver of the invasive phenotype. Here, CTSL is linked to neoplasm.