CSF1R and neoplasm: Likewise, the switching of tumor cell transcriptomics profiles from squamous toward classical GEP has also been observed in different experimental models of PDAC via: (i) inhibition of MET [37] and ZEB1 [86], (ii) blockade of GLI2, OPN, and molecular regulators derived from PSCs [80], and (iii) through depletion of CSF1R+ M2-macrophages (by targeting CSF1R or CXCR2) [88].