Another interesting observation in our study is that neither the over-expression of miR-337-3p nor the specific knockdown of STAT3 and RAP1A significantly decrease cell viability or induce G2/M arrest alone, but rather enhance G2/M arrest and cell death only under conditions of paclitaxel treatment, even though its regulatory targets, STAT3 and RAP1A, have been indicated to promote cancer cell survival and proliferation [50], [51]. The gene discussed is RAP1A; the disease is cancer.