We then performed qPCR and immunocytochemistry for α-SMA, an indicator of myofibroblast differentiation, which showed that enhanced expression of Cacna1c in VICs increased α-SMA by approximately 40% 2 days after infection (Figure 5B) and led to the appearance of α-SMA stress fibers that were not present after control GFP infection (Figure 5C), thus providing initial mechanistic insight into the downstream effects of increased CaV1.2 expression in VICs. The gene discussed is CACNA1C; the disease is infection.