Further studies on several preclinical pancreatic cancer models showed that Meflin expression confers the ability of CAFs to suppress tumour growth, leading to the hypothesis that Meflin is a marker of rCAFs in cancer.9 We further found via a lineage-tracing experiment that Meflin-positive rCAFs are converted into α-SMA-positive CAFs, which presumably represent pCAFs as the tumour grows.9 This indicates the existence of CAF plasticity between rCAFs and pCAFs, which may depend on the tumour microenvironment and context (Fig. 1). This evidence concerns the gene ISLR and neoplasm.