For example, α‐SMA+ myofibroblast‐specific deletion of Col1a1 using a dual recombinase FSF‐KrasG12D/+;Trp53frt/frt;Pdx1‐Flp (KPPF); α‐SMA‐Cre;R26Dual transgenic mouse model resulted in CXCL5 upregulation in cancer cells, leading to augmented recruitment of CD206 + Arg1+ myeloid‐derived suppressor cells (MDSCs), which in turn suppressed CD8+ T cells, leading to aggressive tumours [43]. This evidence concerns the gene ACTA1 and cancer.