Specifically, tumor spheroids were grown within a collagen matrix-incorporated microfluidic chip and co-cultivated with CAFs in a microscale distance away, allowing mutual microenvironmental interactions culminating in CAF activation, as demonstrated by the increase of α-smooth muscle actin (α-SMA) expression and migratory activity, as well as the induction of resistance to the chemotherapeutic paclitaxel (108). Here, ACTA1 is linked to neoplasm.