KRAS and small cell lung carcinoma: Among ROS1-independent mechanisms of resistance, in vivo and in vitro studies have reported acquisition of an activating KIT mutation, the activation of an epithelial-to-mesenchymal transition (EMT), a switch in the control of growth and survival from ROS1 to EGFR, and transformation into small cell lung cancer (SCLC) or KRAS amplifications [44,45,46,47].