Yep, same thing. The esterification of fatty acids just means they have been bonding to an ester to make an acylglycedride - and usually we have 3 bonded to a glycerol make a triglyceride. It's the storage form of fatty acids, and the NEFA form is the ready fuel version.
Non-esterified fatty acids aren't as you say freely roaming as they have to be ported about by proteins. So Non-esterified fatty acids is a more accurate description than Free fatty acids.
Our fat burning cells get them from 3 places;
From inside massive lipoprotein particles called chylomicrons carrying triglyceride from the gut ... will dock with the cell and they will use an enzyme called lipoprotein lipase to break a triglyceride into it's 3 NEFAs and they are transported into the cell.
From inside Low density lipoproteins carrying fat from the liver, much the same process happens to extra a triglyceride out.
Finally when energy in circulation drops, fat cells release NEFAs bound to sheets of protein called albumin and that also carries the NEFAs through the circulation to any consumers. When glucose comes into the system, insulin goes up and that inhibits healthy fat cells from releasing NEFAs into the blood stream. When insulin drops, the fat cells start releasing NEFAs again. That is the daily switch between the fed and fasted state. Insulin going up or down based on when you eat determines if health fat cells release energy.
That is the one Gary Taubes was talking about, when he talks about NEFAS in circulation it's the supply of energy from adipose when glucose is low, to a system that is good at burning fat. That is pretty much Keto perfection in a nutshell.
The problem identified in that paper is a description of what happens when the adipose no longer can store any more energy - which is adipose insulin resistance. The pancreas produces more insulin when there is fat in circulation (to try to get NEFAs out of circulation) when glucose is about - that's one of the drivers of increasing pancreatic over production of insulin, NEFAs and Glucose both in circulation.
Why this is a problem, we have to go down to the level of the cellular consumers of that energy. We have a switch at the mitochondria in our cells where insulin inhibits us being able to quickly get fats in to be burned (the carnitine shuttle). When we have both NEFAs AND glucose (and therefore insulin) in abundance then we burn the glucose and the NEFAs build up in lipid droplets in our cells. Eventually that interferes with the ability to get glucose transports to the cell wall ... and that is cellular IR in action.
I could be wrong about all that ... but that is my understanding. Hope it's helpful.